rabbit anti phospho smad2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti phospho smad2
    Rabbit Anti Phospho Smad2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rabbit anti phospho smad2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti phospho smad2
    Rabbit Anti Phospho Smad2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    phospho smad2 ser465 467  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho smad2 ser465 467
    Cell lysates prepared from ADSCs treated with TGFβ, bFGF or untreated (Unt) were subjected to SDS-PAGE and immunoblotted. (A) 4-day lysates were probed with anti-α-SMA monoclonal antibody or anti-GAPDH antibody as a loading control. Blot is representative of three independent experiments. (B) Lysates prepared at 1 hour of treatment were immunoblotted with <t>anti-phospho-Smad2</t> (pSmad2) and with total Smad antibody. Blot is representative of three independent experiments. Dash represents 37 kD (A) or 50 kD (B). (C, D) After 4 days of treatment, cells were replated onto collagen-coated glass coverslips for two hours before fixation, permeabilization, and staining with anti-vinculin antibody (C, top), rhodamine-phalloidin (C, bottom), or anti-α-SMA monoclonal antibody (D). Insets in (D) show rhodamine-phalloidin staining of the same fields. All images are representative of three independent experiments. Scale bars = 50 µm.
    Phospho Smad2 Ser465 467, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Reversible Modulation of Myofibroblast Differentiation in Adipose-Derived Mesenchymal Stem Cells"

    Article Title: Reversible Modulation of Myofibroblast Differentiation in Adipose-Derived Mesenchymal Stem Cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0086865

    Cell lysates prepared from ADSCs treated with TGFβ, bFGF or untreated (Unt) were subjected to SDS-PAGE and immunoblotted. (A) 4-day lysates were probed with anti-α-SMA monoclonal antibody or anti-GAPDH antibody as a loading control. Blot is representative of three independent experiments. (B) Lysates prepared at 1 hour of treatment were immunoblotted with anti-phospho-Smad2 (pSmad2) and with total Smad antibody. Blot is representative of three independent experiments. Dash represents 37 kD (A) or 50 kD (B). (C, D) After 4 days of treatment, cells were replated onto collagen-coated glass coverslips for two hours before fixation, permeabilization, and staining with anti-vinculin antibody (C, top), rhodamine-phalloidin (C, bottom), or anti-α-SMA monoclonal antibody (D). Insets in (D) show rhodamine-phalloidin staining of the same fields. All images are representative of three independent experiments. Scale bars = 50 µm.
    Figure Legend Snippet: Cell lysates prepared from ADSCs treated with TGFβ, bFGF or untreated (Unt) were subjected to SDS-PAGE and immunoblotted. (A) 4-day lysates were probed with anti-α-SMA monoclonal antibody or anti-GAPDH antibody as a loading control. Blot is representative of three independent experiments. (B) Lysates prepared at 1 hour of treatment were immunoblotted with anti-phospho-Smad2 (pSmad2) and with total Smad antibody. Blot is representative of three independent experiments. Dash represents 37 kD (A) or 50 kD (B). (C, D) After 4 days of treatment, cells were replated onto collagen-coated glass coverslips for two hours before fixation, permeabilization, and staining with anti-vinculin antibody (C, top), rhodamine-phalloidin (C, bottom), or anti-α-SMA monoclonal antibody (D). Insets in (D) show rhodamine-phalloidin staining of the same fields. All images are representative of three independent experiments. Scale bars = 50 µm.

    Techniques Used: SDS Page, Staining

    (A) Lysates were harvested for cells grown as indicated in the legend for lanes 1–4, and immunoblotted with anti-phospho Smad2 or anti-total Smad antibody. GAPDH was used as the loading control. Blot is representative of three independent experiments. (B, C) bFGF, TGF-β receptor inhibitor (TGFβ-RI), or DMSO was added to TGF-β-differentiated ADSCs on day 4. Total RNA was isolated at 6, 24, and 48 hours of treatment and qRT-PCR was performed for type I collagen (B) and tenascin-C (C) expression relative to expression in TGF-β-differentiated ADSCs on day 4, using ubiquitin C as the normalization control. Graphs represent the average of multiple samples from three independent experiments +/− SEM. *p<0.05, **p<0.01, and ***p<0.001. The p-values are for comparisons to expression in TGF-β-differentiated ADSCs, unless otherwise indicated.
    Figure Legend Snippet: (A) Lysates were harvested for cells grown as indicated in the legend for lanes 1–4, and immunoblotted with anti-phospho Smad2 or anti-total Smad antibody. GAPDH was used as the loading control. Blot is representative of three independent experiments. (B, C) bFGF, TGF-β receptor inhibitor (TGFβ-RI), or DMSO was added to TGF-β-differentiated ADSCs on day 4. Total RNA was isolated at 6, 24, and 48 hours of treatment and qRT-PCR was performed for type I collagen (B) and tenascin-C (C) expression relative to expression in TGF-β-differentiated ADSCs on day 4, using ubiquitin C as the normalization control. Graphs represent the average of multiple samples from three independent experiments +/− SEM. *p<0.05, **p<0.01, and ***p<0.001. The p-values are for comparisons to expression in TGF-β-differentiated ADSCs, unless otherwise indicated.

    Techniques Used: Isolation, Quantitative RT-PCR, Expressing

    (A) The % contraction of fibrin-fibronectin matrices by differentiated and re-differentiated cells was averaged for 6–14 total reactions (+/− SEM) from three independent experiments. **p<0.01, ***p<0.001 (B) A Transwell migration assay was performed with re-differentiated cells. Unt, bFGF, and TGFβ data are from . Quantification represents the average number of cells per field +/− SEM from three to four independent experiments. **p<0.01, ***p<0.001. (C) Comparison of myofibroblast and fibroblast features. TGF-β-differentiated ADSCs are myofibroblastic, contractile, and produce increased type I collagen, fibronectin, α-SMA, and phospho-Smad2. Fibroblast-like cells lack myofibroblastic features, are more migratory, and have increased levels of tenascin-C, vimentin, and phospho-ERK1/2. These fibroblastic and myofibroblastic phenotypes are not terminal and are reversed by switching the respective growth factor treatments.
    Figure Legend Snippet: (A) The % contraction of fibrin-fibronectin matrices by differentiated and re-differentiated cells was averaged for 6–14 total reactions (+/− SEM) from three independent experiments. **p<0.01, ***p<0.001 (B) A Transwell migration assay was performed with re-differentiated cells. Unt, bFGF, and TGFβ data are from . Quantification represents the average number of cells per field +/− SEM from three to four independent experiments. **p<0.01, ***p<0.001. (C) Comparison of myofibroblast and fibroblast features. TGF-β-differentiated ADSCs are myofibroblastic, contractile, and produce increased type I collagen, fibronectin, α-SMA, and phospho-Smad2. Fibroblast-like cells lack myofibroblastic features, are more migratory, and have increased levels of tenascin-C, vimentin, and phospho-ERK1/2. These fibroblastic and myofibroblastic phenotypes are not terminal and are reversed by switching the respective growth factor treatments.

    Techniques Used: Transwell Migration Assay

    phosphorylated smad2 3  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylated smad2 3
    Phosphorylated Smad2 3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rabbit anti phospho smad2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti phospho smad2
    A. The expression of TβRII was detected by Western blot. B. Fibroblasts were exposed to SW620-S for 0, 2, 4 and 6 days, and <t>p-Smad2</t> was detected by Western blot. The protein levels were normalized to that of β-actin in the same cell extracts. C.D. Fibroblasts were exposed to SW620-S or TGF-β1 in the presence of 10 µM SB431542 for 6 days, and IGFBP7 mRNA expression was detected by RT-PCR (C) and Q-PCR (D). The mRNA level was normalized to that of GAPDH in the same cell extracts. E. Fibroblasts were exposed to SW620-S or TGF-β1 with 10 µM SB431542 for 6 days, and the expression of Smad2, p-Smad2 (E) was detected by Western blot. The protein levels were normalized to that of β-actin in the same cell extracts. * P <0.05 between SW620-S/TGF-β1-treated fibroblasts and control group. + P <0.05 between SW620-S-treated fibroblasts with or without SB431542, # P <0.05 between TGF-β1-treated fibroblasts with or without SB431542.
    Rabbit Anti Phospho Smad2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "High Expression of IGFBP7 in Fibroblasts Induced by Colorectal Cancer Cells Is Co-Regulated by TGF-β and Wnt Signaling in a Smad2/3-Dvl2/3-Dependent Manner"

    Article Title: High Expression of IGFBP7 in Fibroblasts Induced by Colorectal Cancer Cells Is Co-Regulated by TGF-β and Wnt Signaling in a Smad2/3-Dvl2/3-Dependent Manner

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0085340

    A. The expression of TβRII was detected by Western blot. B. Fibroblasts were exposed to SW620-S for 0, 2, 4 and 6 days, and p-Smad2 was detected by Western blot. The protein levels were normalized to that of β-actin in the same cell extracts. C.D. Fibroblasts were exposed to SW620-S or TGF-β1 in the presence of 10 µM SB431542 for 6 days, and IGFBP7 mRNA expression was detected by RT-PCR (C) and Q-PCR (D). The mRNA level was normalized to that of GAPDH in the same cell extracts. E. Fibroblasts were exposed to SW620-S or TGF-β1 with 10 µM SB431542 for 6 days, and the expression of Smad2, p-Smad2 (E) was detected by Western blot. The protein levels were normalized to that of β-actin in the same cell extracts. * P <0.05 between SW620-S/TGF-β1-treated fibroblasts and control group. + P <0.05 between SW620-S-treated fibroblasts with or without SB431542, # P <0.05 between TGF-β1-treated fibroblasts with or without SB431542.
    Figure Legend Snippet: A. The expression of TβRII was detected by Western blot. B. Fibroblasts were exposed to SW620-S for 0, 2, 4 and 6 days, and p-Smad2 was detected by Western blot. The protein levels were normalized to that of β-actin in the same cell extracts. C.D. Fibroblasts were exposed to SW620-S or TGF-β1 in the presence of 10 µM SB431542 for 6 days, and IGFBP7 mRNA expression was detected by RT-PCR (C) and Q-PCR (D). The mRNA level was normalized to that of GAPDH in the same cell extracts. E. Fibroblasts were exposed to SW620-S or TGF-β1 with 10 µM SB431542 for 6 days, and the expression of Smad2, p-Smad2 (E) was detected by Western blot. The protein levels were normalized to that of β-actin in the same cell extracts. * P <0.05 between SW620-S/TGF-β1-treated fibroblasts and control group. + P <0.05 between SW620-S-treated fibroblasts with or without SB431542, # P <0.05 between TGF-β1-treated fibroblasts with or without SB431542.

    Techniques Used: Expressing, Western Blot, Reverse Transcription Polymerase Chain Reaction

    A-D. Fibroblasts were exposed to SW620-S or TGF-β1 in the presence of 10 µM SB431542 for 6days, and the mRNA expression of the Wnt signal target genes c-Myc (A), CCND1 (B) and DKK1 (C) were assessed by Q-PCR. mRNA expression was normalized to that of GAPDH in the same cell extracts. The expression of Dvl3 was detected by Western blot (D). Protein expression was normalized to that of β-actin in the same cell extract. * P <0.05 between SW620-S-treated fibroblasts and control group. ** P <0.05 between TGF-β1-treated fibroblasts and control group. + P <0.05 between SW620-S-treated fibroblasts with or without SB431542. # P <0.05 between TGF-β1-treated fibroblasts with or without SB431542. E. Model of high expression of IGFBP7 induced by the tumor cell-fibroblast interactions. F. TGF-β signal activation up-regulates Smad2/3 and Dvl2/3, accompanied by up-regulation of the Wnt target genes c-Myc, CCND1 and DKK1, such that IGFBP7 is over-expressed.
    Figure Legend Snippet: A-D. Fibroblasts were exposed to SW620-S or TGF-β1 in the presence of 10 µM SB431542 for 6days, and the mRNA expression of the Wnt signal target genes c-Myc (A), CCND1 (B) and DKK1 (C) were assessed by Q-PCR. mRNA expression was normalized to that of GAPDH in the same cell extracts. The expression of Dvl3 was detected by Western blot (D). Protein expression was normalized to that of β-actin in the same cell extract. * P <0.05 between SW620-S-treated fibroblasts and control group. ** P <0.05 between TGF-β1-treated fibroblasts and control group. + P <0.05 between SW620-S-treated fibroblasts with or without SB431542. # P <0.05 between TGF-β1-treated fibroblasts with or without SB431542. E. Model of high expression of IGFBP7 induced by the tumor cell-fibroblast interactions. F. TGF-β signal activation up-regulates Smad2/3 and Dvl2/3, accompanied by up-regulation of the Wnt target genes c-Myc, CCND1 and DKK1, such that IGFBP7 is over-expressed.

    Techniques Used: Expressing, Western Blot, Activation Assay

    psmad2 3  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc psmad2 3
    Serelaxin reactivates Rxfp1 expression via histone modifications. (A) Schematic representing the mouse Rxfp1 locus with locations of CHIP-qPCR primers. (B) qPCR analysis showing the enrichment of 4 different histone modification marks (active: H3K4me3 and H3K27ac, repressive: H3K9me3, H3K27me3) in the Rxfp1 promoter region (Amplicon 1-3) and intron 10 (Amplicon 4). The enrichment of TGFβ1-influenced H3K4me3, H3K9me3 and H3K27me3 marks were significantly compromised by Serelaxin if performed with amplicons 1-3 targeting the promoter region but not with amplicon 4 targeting intron10. (C) ChIP-qPCR analysis showing the enrichment of histone modification marks in the Rxfp1 promoter region after RXFP1 knockdown. Upon RXFP1 knockdown, treatment with Serelaxin did not significantly increase the activating modifications or decrease the repressive modification marks. (D) Western blot analysis showing protein levels of <t>pSMAD2</t> and pSMAD3 in sham, AAC-operated and AAC-operated+Serelaxin-treated mouse hearts, total SMAD2 and SMAD3 were used as protein loading controls. AAC-operated hearts showed increased levels of pSMAD2 and pSMAD3 compared to sham. Upon treatment with Serelaxin these protein levels were significantly reduced. (E) qPCR analysis showing the enrichment of <t>pSMAD2/3</t> in the Rxfp1 promoter region (Amplicon 2) and intron 10 (Amplicon 4). The enrichment of TGFβ1-induced pSMAD2/3 was significantly compromised by Serelaxin. The qPCR analysis with primer targeting intron10 did not show any significant differences between these groups. Student t-test was used for single comparison and one-way ANOVA with Bonferroni post-hoc analysis was used for multiple group comparisons. Gene expression and associated error bars, representing mean ± SEM, n≥3, n.s. no significance, ** p<0.01, *** p<0.001, **** p<0.0001.
    Psmad2 3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Serelaxin alleviates cardiac fibrosis through inhibiting endothelial-to-mesenchymal transition via RXFP1"

    Article Title: Serelaxin alleviates cardiac fibrosis through inhibiting endothelial-to-mesenchymal transition via RXFP1

    Journal: Theranostics

    doi: 10.7150/thno.38640

    Serelaxin reactivates Rxfp1 expression via histone modifications. (A) Schematic representing the mouse Rxfp1 locus with locations of CHIP-qPCR primers. (B) qPCR analysis showing the enrichment of 4 different histone modification marks (active: H3K4me3 and H3K27ac, repressive: H3K9me3, H3K27me3) in the Rxfp1 promoter region (Amplicon 1-3) and intron 10 (Amplicon 4). The enrichment of TGFβ1-influenced H3K4me3, H3K9me3 and H3K27me3 marks were significantly compromised by Serelaxin if performed with amplicons 1-3 targeting the promoter region but not with amplicon 4 targeting intron10. (C) ChIP-qPCR analysis showing the enrichment of histone modification marks in the Rxfp1 promoter region after RXFP1 knockdown. Upon RXFP1 knockdown, treatment with Serelaxin did not significantly increase the activating modifications or decrease the repressive modification marks. (D) Western blot analysis showing protein levels of pSMAD2 and pSMAD3 in sham, AAC-operated and AAC-operated+Serelaxin-treated mouse hearts, total SMAD2 and SMAD3 were used as protein loading controls. AAC-operated hearts showed increased levels of pSMAD2 and pSMAD3 compared to sham. Upon treatment with Serelaxin these protein levels were significantly reduced. (E) qPCR analysis showing the enrichment of pSMAD2/3 in the Rxfp1 promoter region (Amplicon 2) and intron 10 (Amplicon 4). The enrichment of TGFβ1-induced pSMAD2/3 was significantly compromised by Serelaxin. The qPCR analysis with primer targeting intron10 did not show any significant differences between these groups. Student t-test was used for single comparison and one-way ANOVA with Bonferroni post-hoc analysis was used for multiple group comparisons. Gene expression and associated error bars, representing mean ± SEM, n≥3, n.s. no significance, ** p<0.01, *** p<0.001, **** p<0.0001.
    Figure Legend Snippet: Serelaxin reactivates Rxfp1 expression via histone modifications. (A) Schematic representing the mouse Rxfp1 locus with locations of CHIP-qPCR primers. (B) qPCR analysis showing the enrichment of 4 different histone modification marks (active: H3K4me3 and H3K27ac, repressive: H3K9me3, H3K27me3) in the Rxfp1 promoter region (Amplicon 1-3) and intron 10 (Amplicon 4). The enrichment of TGFβ1-influenced H3K4me3, H3K9me3 and H3K27me3 marks were significantly compromised by Serelaxin if performed with amplicons 1-3 targeting the promoter region but not with amplicon 4 targeting intron10. (C) ChIP-qPCR analysis showing the enrichment of histone modification marks in the Rxfp1 promoter region after RXFP1 knockdown. Upon RXFP1 knockdown, treatment with Serelaxin did not significantly increase the activating modifications or decrease the repressive modification marks. (D) Western blot analysis showing protein levels of pSMAD2 and pSMAD3 in sham, AAC-operated and AAC-operated+Serelaxin-treated mouse hearts, total SMAD2 and SMAD3 were used as protein loading controls. AAC-operated hearts showed increased levels of pSMAD2 and pSMAD3 compared to sham. Upon treatment with Serelaxin these protein levels were significantly reduced. (E) qPCR analysis showing the enrichment of pSMAD2/3 in the Rxfp1 promoter region (Amplicon 2) and intron 10 (Amplicon 4). The enrichment of TGFβ1-induced pSMAD2/3 was significantly compromised by Serelaxin. The qPCR analysis with primer targeting intron10 did not show any significant differences between these groups. Student t-test was used for single comparison and one-way ANOVA with Bonferroni post-hoc analysis was used for multiple group comparisons. Gene expression and associated error bars, representing mean ± SEM, n≥3, n.s. no significance, ** p<0.01, *** p<0.001, **** p<0.0001.

    Techniques Used: Expressing, Modification, Amplification, Western Blot

    Antibodies used in ChIP-qPCR
    Figure Legend Snippet: Antibodies used in ChIP-qPCR

    Techniques Used:

    smad2 3 pakt  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc smad2 3 pakt
    A., and <t>Smad2</t> and Smad3 mRNA B. ; and TMEPAI mRNA C. in human normal mammary epithelial cells (HMEC) and various triple negative breast cancer cell lines (MDA-MB-231, BT20, HCC1937, MDA-MB-157, Hs578T) along with TMEPAI knockdown MDA-MB-231 cells (231-TMKD/TMKD).
    Smad2 3 Pakt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Increased Smad3 and reduced Smad2 levels mediate the functional switch of TGF-β from growth suppressor to growth and metastasis promoter through TMEPAI/PMEPA1 in triple negative breast cancer"

    Article Title: Increased Smad3 and reduced Smad2 levels mediate the functional switch of TGF-β from growth suppressor to growth and metastasis promoter through TMEPAI/PMEPA1 in triple negative breast cancer

    Journal: Genes & Cancer

    doi: 10.18632/genesandcancer.194

    A., and Smad2 and Smad3 mRNA B. ; and TMEPAI mRNA C. in human normal mammary epithelial cells (HMEC) and various triple negative breast cancer cell lines (MDA-MB-231, BT20, HCC1937, MDA-MB-157, Hs578T) along with TMEPAI knockdown MDA-MB-231 cells (231-TMKD/TMKD).
    Figure Legend Snippet: A., and Smad2 and Smad3 mRNA B. ; and TMEPAI mRNA C. in human normal mammary epithelial cells (HMEC) and various triple negative breast cancer cell lines (MDA-MB-231, BT20, HCC1937, MDA-MB-157, Hs578T) along with TMEPAI knockdown MDA-MB-231 cells (231-TMKD/TMKD).

    Techniques Used:

    A. Relative levels of Smad2, Smad3, TMEPAI and GAPDH in MDA-MB-231 cells expressing control shRNA, Smad2 shRNA and Smad3 shRNA. B.-E. Growth curves of MDA-MB-231 cells expressing control shRNA (B), Smad2 shRNA (C), Smad3 shRNA (D) and TMEPAI shRNA (E) in the absence or presence of TGF-β (2 ng/ml).
    Figure Legend Snippet: A. Relative levels of Smad2, Smad3, TMEPAI and GAPDH in MDA-MB-231 cells expressing control shRNA, Smad2 shRNA and Smad3 shRNA. B.-E. Growth curves of MDA-MB-231 cells expressing control shRNA (B), Smad2 shRNA (C), Smad3 shRNA (D) and TMEPAI shRNA (E) in the absence or presence of TGF-β (2 ng/ml).

    Techniques Used: Expressing, shRNA

    A. Relative expression of phospho Smad2/3, Total Smad2/3 and TMEPAI in MDA-MB-231 cells expressing Con shRNA, Smad2 shRNA and Smad3 shRNA in the absence or presence of TGF-β (2 ng/ml), B. Relative levels of TMEPAI mRNAs in human mammary epithelial cells (HME) and MDA-MB-231 cells that are expressing Con shRNA, TMEPAI shRNA (TMKD), Smad2 shRNA (Smad2KD) or Smad3 shRNA (Smad3KD) in the absence or presence of TGF-β (2 ng/ml), C. 12XCAGA-Luc reporter activity in MDA-MB-231 cells expressing Con ShRNA, Smad2 shRNA, Smad3 shRNA both in the absence or presence of TGF-β (2 ng/ml). D. 3XARE-Luc reporter activity in MDA-MB-231 cells expressing Con ShRNA, Smad2 shRNA, Smad3 shRNA both in the absence or presence of TGF-β (2 ng/ml). E. 12xCAGA-Luc reporter activity in MDA-MB-231 cells expressing Con ShRNA (231_CON) and TMEPAI shRNA (231_TMKD) in the absence or presence of TGF-β (2 ng/ml). F. 3XARE-Luc reporter activity in MDA-MB-231 cells expressing Con ShRNA (231_CON) and TMEPAI shRNA (231_TMKD) in the absence or presence of TGF-β (2 ng/ml). G. Schematic representation of three different size TMEPAI promoters tagged with luciferase reporter (−2251-Luc, −973-Luc, −301-Luc) and corresponding luciferase reporter activities in MDA-MB-231 cells in the absence or presence of TGF-β (2 ng/ml). H. TMEPAI promoter activity in MDA-MB-231 cells expressing con shRNA, Smad2 shRNA, and Smad3 shRNA in the absence or presence of TGF-β (2 ng/ml) using 2251 bp TMEPAI promoter (−2251-Luc).
    Figure Legend Snippet: A. Relative expression of phospho Smad2/3, Total Smad2/3 and TMEPAI in MDA-MB-231 cells expressing Con shRNA, Smad2 shRNA and Smad3 shRNA in the absence or presence of TGF-β (2 ng/ml), B. Relative levels of TMEPAI mRNAs in human mammary epithelial cells (HME) and MDA-MB-231 cells that are expressing Con shRNA, TMEPAI shRNA (TMKD), Smad2 shRNA (Smad2KD) or Smad3 shRNA (Smad3KD) in the absence or presence of TGF-β (2 ng/ml), C. 12XCAGA-Luc reporter activity in MDA-MB-231 cells expressing Con ShRNA, Smad2 shRNA, Smad3 shRNA both in the absence or presence of TGF-β (2 ng/ml). D. 3XARE-Luc reporter activity in MDA-MB-231 cells expressing Con ShRNA, Smad2 shRNA, Smad3 shRNA both in the absence or presence of TGF-β (2 ng/ml). E. 12xCAGA-Luc reporter activity in MDA-MB-231 cells expressing Con ShRNA (231_CON) and TMEPAI shRNA (231_TMKD) in the absence or presence of TGF-β (2 ng/ml). F. 3XARE-Luc reporter activity in MDA-MB-231 cells expressing Con ShRNA (231_CON) and TMEPAI shRNA (231_TMKD) in the absence or presence of TGF-β (2 ng/ml). G. Schematic representation of three different size TMEPAI promoters tagged with luciferase reporter (−2251-Luc, −973-Luc, −301-Luc) and corresponding luciferase reporter activities in MDA-MB-231 cells in the absence or presence of TGF-β (2 ng/ml). H. TMEPAI promoter activity in MDA-MB-231 cells expressing con shRNA, Smad2 shRNA, and Smad3 shRNA in the absence or presence of TGF-β (2 ng/ml) using 2251 bp TMEPAI promoter (−2251-Luc).

    Techniques Used: Expressing, shRNA, Activity Assay, Luciferase

    A. Growth curves of MDA-MB-231 cells expressing control shRNA (CON shRNA), Smad2 shRNA, Smad3 shRNA or Smad3shRNA along with human TMEPAI cDNA (Smad3 shRNA+hTM) in the absence or presence of TGF-β (2 ng/ml). B. Relative expression of phosphorylated Akt (pAkt), Smad2, Smad3, Snail, Slug, PTEN, p27 and TMEPAI in MDA-MB-231 cells expressing Con shRNA (CON), Smad2 shRNA (S2KD), Smad3 shRNA (S3KD) and Smad3 shRNA along with human TMEPAI cDNA (S3KD+hTM) in the absence or presence of TGF-β (2 ng/ml). Phase contrast images of toluidine blue stained transit well invasion assay (C) and relative invasion index (D) of MDA-MB-231 cells expressing control shRNA (CON shRNA), Smad2 shRNA, Smad3 shRNA and Smad3shRNA along with human TMEPAI cDNA in the absence or presence of TGF-β (2 ng/ml).
    Figure Legend Snippet: A. Growth curves of MDA-MB-231 cells expressing control shRNA (CON shRNA), Smad2 shRNA, Smad3 shRNA or Smad3shRNA along with human TMEPAI cDNA (Smad3 shRNA+hTM) in the absence or presence of TGF-β (2 ng/ml). B. Relative expression of phosphorylated Akt (pAkt), Smad2, Smad3, Snail, Slug, PTEN, p27 and TMEPAI in MDA-MB-231 cells expressing Con shRNA (CON), Smad2 shRNA (S2KD), Smad3 shRNA (S3KD) and Smad3 shRNA along with human TMEPAI cDNA (S3KD+hTM) in the absence or presence of TGF-β (2 ng/ml). Phase contrast images of toluidine blue stained transit well invasion assay (C) and relative invasion index (D) of MDA-MB-231 cells expressing control shRNA (CON shRNA), Smad2 shRNA, Smad3 shRNA and Smad3shRNA along with human TMEPAI cDNA in the absence or presence of TGF-β (2 ng/ml).

    Techniques Used: Expressing, shRNA, Staining, Invasion Assay

    Relative mRNA expression of Smad2 A. , Smad3 B. , TMEPAI C. , Snai1 D. , Slug E. in MDA-MB-231 (231) cells that are expressing control, TMEPAI (TMKD), Smad2 (Smad2KD) and Smad3 (Smad3KD) shRNAs in the absence or presence of TGF-β (2 ng/ml) relative to normal human mammary epithelial cells (HMEC).
    Figure Legend Snippet: Relative mRNA expression of Smad2 A. , Smad3 B. , TMEPAI C. , Snai1 D. , Slug E. in MDA-MB-231 (231) cells that are expressing control, TMEPAI (TMKD), Smad2 (Smad2KD) and Smad3 (Smad3KD) shRNAs in the absence or presence of TGF-β (2 ng/ml) relative to normal human mammary epithelial cells (HMEC).

    Techniques Used: Expressing

    A. Relative expression of Smad2, Smad3 and TMEPAI in Control (HCC), Smad2 knockdown (S2KD) and Smad3 knockdown (S3KD) HCC1937 TNBC cells. B. Growth of control HCC1937 (HCC) in the presence and absence of TGF-β. C. Growth of Smad2 knockdown HCC1937 (S2KD) in the presence and absence of TGF-β. D. Growth of Smad3 knockdown HCC1937 (S3KD) in the presence and absence of TGF-β. E. Relative expressions of E-Cad, Snail and Slug in control (CON) and TMEPAI knockdown (TMKD) HCC1937 cells. F. Relative expressions of E-Cad and Vimentin in control (CON), Smad2 knockdown (S2KD) and Smad3 knockdown (S3KD) HCC1937 cells.
    Figure Legend Snippet: A. Relative expression of Smad2, Smad3 and TMEPAI in Control (HCC), Smad2 knockdown (S2KD) and Smad3 knockdown (S3KD) HCC1937 TNBC cells. B. Growth of control HCC1937 (HCC) in the presence and absence of TGF-β. C. Growth of Smad2 knockdown HCC1937 (S2KD) in the presence and absence of TGF-β. D. Growth of Smad3 knockdown HCC1937 (S3KD) in the presence and absence of TGF-β. E. Relative expressions of E-Cad, Snail and Slug in control (CON) and TMEPAI knockdown (TMKD) HCC1937 cells. F. Relative expressions of E-Cad and Vimentin in control (CON), Smad2 knockdown (S2KD) and Smad3 knockdown (S3KD) HCC1937 cells.

    Techniques Used: Expressing

    Kaplan Meier curves for overall survival of triple negative breast cancer patients in relation to expression of TMEPAI/PMEPA1 (A), Smad2 (B), Smad3 (C) or Smad4 (D) mRNA using a publicly accessible database (GSE58812). E. Western blots of TMEPAI and total Smad2/3 proteins in primary tumors from human breast cancer patients (BC1- BC5) and corresponding normal/benign (N1-N4) samples relative to MDA-MB-231 cells (231).
    Figure Legend Snippet: Kaplan Meier curves for overall survival of triple negative breast cancer patients in relation to expression of TMEPAI/PMEPA1 (A), Smad2 (B), Smad3 (C) or Smad4 (D) mRNA using a publicly accessible database (GSE58812). E. Western blots of TMEPAI and total Smad2/3 proteins in primary tumors from human breast cancer patients (BC1- BC5) and corresponding normal/benign (N1-N4) samples relative to MDA-MB-231 cells (231).

    Techniques Used: Expressing, Western Blot

    The data demonstrate that the consequences of switch from Smad2 to Smad3 signaling pathway results in converting TGF-β from tumor suppressor to pro-oncogene as cells acquire increasing malignant properties through Smad3 mediated TMEPAI expression.
    Figure Legend Snippet: The data demonstrate that the consequences of switch from Smad2 to Smad3 signaling pathway results in converting TGF-β from tumor suppressor to pro-oncogene as cells acquire increasing malignant properties through Smad3 mediated TMEPAI expression.

    Techniques Used: Expressing

    phospho smad 3 ser423 425  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho smad 3 ser423 425
    Phospho Smad 3 Ser423 425, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti phospho smad2 3  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti phospho smad2 3
    PCI34051 alleviates cardiac fibrosis in transverse aortic constriction (TAC) mice through the TGF- β <t>1-Smad2/3</t> pathway. (a, b) Picrosirius red staining of mouse cardiac tissues; representative images and quantification are shown. Scale bar = 50 μ m. The expression levels of the fibrosis marker genes Col1a1 (c), Fn1 (d), Acta2 (e), and Tgfb1 (f) were determined using quantitative real-time polymerase chain reaction ( n = 5–6 per group). (g) The cardiac expression levels of Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 were analyzed using western blotting. Actb was used as a loading control. Representative blots are shown. (h–k) Quantification of Fn1, Acta2, Tgfb1, and p-Smad2/3 to Smad2/3 ( n = 5–6 per group).
    Anti Phospho Smad2 3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Hdac8 Inhibitor Alleviates Transverse Aortic Constriction-Induced Heart Failure in Mice by Downregulating Ace1"

    Article Title: Hdac8 Inhibitor Alleviates Transverse Aortic Constriction-Induced Heart Failure in Mice by Downregulating Ace1

    Journal: Oxidative Medicine and Cellular Longevity

    doi: 10.1155/2022/6227330

    PCI34051 alleviates cardiac fibrosis in transverse aortic constriction (TAC) mice through the TGF- β 1-Smad2/3 pathway. (a, b) Picrosirius red staining of mouse cardiac tissues; representative images and quantification are shown. Scale bar = 50 μ m. The expression levels of the fibrosis marker genes Col1a1 (c), Fn1 (d), Acta2 (e), and Tgfb1 (f) were determined using quantitative real-time polymerase chain reaction ( n = 5–6 per group). (g) The cardiac expression levels of Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 were analyzed using western blotting. Actb was used as a loading control. Representative blots are shown. (h–k) Quantification of Fn1, Acta2, Tgfb1, and p-Smad2/3 to Smad2/3 ( n = 5–6 per group).
    Figure Legend Snippet: PCI34051 alleviates cardiac fibrosis in transverse aortic constriction (TAC) mice through the TGF- β 1-Smad2/3 pathway. (a, b) Picrosirius red staining of mouse cardiac tissues; representative images and quantification are shown. Scale bar = 50 μ m. The expression levels of the fibrosis marker genes Col1a1 (c), Fn1 (d), Acta2 (e), and Tgfb1 (f) were determined using quantitative real-time polymerase chain reaction ( n = 5–6 per group). (g) The cardiac expression levels of Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 were analyzed using western blotting. Actb was used as a loading control. Representative blots are shown. (h–k) Quantification of Fn1, Acta2, Tgfb1, and p-Smad2/3 to Smad2/3 ( n = 5–6 per group).

    Techniques Used: Staining, Expressing, Marker, Real-time Polymerase Chain Reaction, Western Blot

    PCI34051 alleviates pulmonary congestion and fibrosis in transverse aortic constriction (TAC) mice. (a) The ratio of lung weight-to-bodyweight (LW/BW) in the sham+vehicle, sham+PCI34051 (10 mg/kg bodyweight/day), TAC+vehicle, and TAC+PCI34051 (3, 10, or 30 mg/kg bodyweight/day) groups ( n = 5–6 per group) was determined. Representative images of mouse lungs (B). (b) Representative images of pulmonary tissues stained with hematoxylin and eosin. Scale bar = 50 μ m. (c) Representative images of pulmonary tissues stained with Picrosirius red. Scale bar = 50 μ m. (d) Pulmonary fibrosis was quantified using ImageJ software. (e–h) The mRNA levels of Col1a1 , Fn1 , Acta2 , and Tgfb1 were evaluated using quantitative real-time polymerase chain reaction ( n = 5–6 per group). (i–m) Representative western blots and quantification of Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 levels in the pulmonary tissues ( n = 5–6 per group).
    Figure Legend Snippet: PCI34051 alleviates pulmonary congestion and fibrosis in transverse aortic constriction (TAC) mice. (a) The ratio of lung weight-to-bodyweight (LW/BW) in the sham+vehicle, sham+PCI34051 (10 mg/kg bodyweight/day), TAC+vehicle, and TAC+PCI34051 (3, 10, or 30 mg/kg bodyweight/day) groups ( n = 5–6 per group) was determined. Representative images of mouse lungs (B). (b) Representative images of pulmonary tissues stained with hematoxylin and eosin. Scale bar = 50 μ m. (c) Representative images of pulmonary tissues stained with Picrosirius red. Scale bar = 50 μ m. (d) Pulmonary fibrosis was quantified using ImageJ software. (e–h) The mRNA levels of Col1a1 , Fn1 , Acta2 , and Tgfb1 were evaluated using quantitative real-time polymerase chain reaction ( n = 5–6 per group). (i–m) Representative western blots and quantification of Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 levels in the pulmonary tissues ( n = 5–6 per group).

    Techniques Used: Staining, Software, Real-time Polymerase Chain Reaction, Western Blot

    PCI34051 or Hdac8 knockdown mitigates TGF- β 1-induced fibrosis in rat cardiac fibroblasts. (a–e) Rat cardiac fibroblasts were pre-treated with TGF– β 1 (10 ng/mL) for 1 h and cultured in the presence of vehicle or PCI34051 (10 μ M) for 8 h. mRNA levels of Hdac8 , Col1a1 , Fn1 , Acta2 , and Tgfb1 were evaluated using quantitative real-time polymerase chain reaction (qRT-PCR) ( n = 4–6 per group). (f–k) Representative immunoblots and quantification of Hdac8, Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 levels in rat cardiac fibroblasts ( n = 6 per group). Actb was used as a loading control. (l–p) Rat cardiac fibroblasts were transfected with control or short-interfering RNA against Hdac8 and treated with TGF- β 1 (10 ng/mL) for 9 h. The mRNA levels of Hdac8 , Fn1 , Acta2 , Tgfb1 , and Ace1 were determined using qRT-PCR ( n = 5 per group). (q–w) Representative immunoblots and quantification of Hdac8, Ace1, Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 levels in rat cardiac fibroblasts ( n = 4 per group). Actb was used as a loading control.
    Figure Legend Snippet: PCI34051 or Hdac8 knockdown mitigates TGF- β 1-induced fibrosis in rat cardiac fibroblasts. (a–e) Rat cardiac fibroblasts were pre-treated with TGF– β 1 (10 ng/mL) for 1 h and cultured in the presence of vehicle or PCI34051 (10 μ M) for 8 h. mRNA levels of Hdac8 , Col1a1 , Fn1 , Acta2 , and Tgfb1 were evaluated using quantitative real-time polymerase chain reaction (qRT-PCR) ( n = 4–6 per group). (f–k) Representative immunoblots and quantification of Hdac8, Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 levels in rat cardiac fibroblasts ( n = 6 per group). Actb was used as a loading control. (l–p) Rat cardiac fibroblasts were transfected with control or short-interfering RNA against Hdac8 and treated with TGF- β 1 (10 ng/mL) for 9 h. The mRNA levels of Hdac8 , Fn1 , Acta2 , Tgfb1 , and Ace1 were determined using qRT-PCR ( n = 5 per group). (q–w) Representative immunoblots and quantification of Hdac8, Ace1, Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 levels in rat cardiac fibroblasts ( n = 4 per group). Actb was used as a loading control.

    Techniques Used: Cell Culture, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Western Blot, Transfection, Small Interfering RNA

    Suppression of HDAC8 attenuates fibrosis, inflammation, cardiac dysfunction, and pulmonary congestion in heart failure. Schematic diagram depicting the Hdac8 selective inhibitor- (PCI34051-) mediated or Hdac8 short-interfering RNA-mediated inhibition of transverse aortic constriction- (TAC-) induced heart failure. TAC-mediated pressure overload upregulates the expression of Hdac8 and Ace1 and downregulates the expression of Ace2 in the heart and lungs. In cardiomyocytes, overexpression of Hdac8 upregulates the expression of Ace1 and downregulates the expression of Ace2. PCI34051 treatment or Hdac8 knockdown mitigates TGF- β 1-induced upregulation of p-Smad2/3, Col1a1, Fn1, and Acta2 in vitro. PCI34051 regulates the TNF α -mediated or Ace1 overexpression-mediated expression of Rela and Nfkbia. PCI34051 alleviates cardiac hypertrophy and dysfunction, inflammation, fibrosis, and pulmonary congestion in heart failure.
    Figure Legend Snippet: Suppression of HDAC8 attenuates fibrosis, inflammation, cardiac dysfunction, and pulmonary congestion in heart failure. Schematic diagram depicting the Hdac8 selective inhibitor- (PCI34051-) mediated or Hdac8 short-interfering RNA-mediated inhibition of transverse aortic constriction- (TAC-) induced heart failure. TAC-mediated pressure overload upregulates the expression of Hdac8 and Ace1 and downregulates the expression of Ace2 in the heart and lungs. In cardiomyocytes, overexpression of Hdac8 upregulates the expression of Ace1 and downregulates the expression of Ace2. PCI34051 treatment or Hdac8 knockdown mitigates TGF- β 1-induced upregulation of p-Smad2/3, Col1a1, Fn1, and Acta2 in vitro. PCI34051 regulates the TNF α -mediated or Ace1 overexpression-mediated expression of Rela and Nfkbia. PCI34051 alleviates cardiac hypertrophy and dysfunction, inflammation, fibrosis, and pulmonary congestion in heart failure.

    Techniques Used: Small Interfering RNA, Inhibition, Expressing, Over Expression, In Vitro

    p smad2 3  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p smad2 3
    RAGE deficiency induces age-associated TGF-β signaling. (A) Relative expression of Tgfb1 gene. Young WT n=4, Young Rage-/- n=4-5, Middle-age (MA) WT n=4, MA Rage-/- n=4, Old WT n=5, Old Rage-/- n=6. (B) (Left panel) Representative images of LV sections stained with an <t>anti-Smad2-3</t> antibody. Bar, 20 µm. (Right panel) Quantification of Smad2/3 signal. Young WT n=5, Young Rage-/- n=5, MA WT n=4, MA Rage-/- n=4, Old WT n=4, Old Rage-/- n=5. (C) (Left panel) Representative images of LV sections stained with an anti-TFGbetaR1 antibody. Bar, 20 µm. (Right panel) Quantification of TFGbetaR1 signal. Young WT n=5, Young Rage-/- n=5, MA WT n=4, MA Rage-/- n=4, Old WT n=4, Old Rage-/- n=5. Each dot represents a mouse; mean ± SD are shown (*, P<0.05; **, P<0.01; ***, P<0.001; 2-way ANOVA plus Bonferroni post-hoc test for multiple comparisons).
    P Smad2 3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Soluble Receptor for Advanced Glycation End-products regulates age-associated Cardiac Fibrosis"

    Article Title: Soluble Receptor for Advanced Glycation End-products regulates age-associated Cardiac Fibrosis

    Journal: International Journal of Biological Sciences

    doi: 10.7150/ijbs.56379

    RAGE deficiency induces age-associated TGF-β signaling. (A) Relative expression of Tgfb1 gene. Young WT n=4, Young Rage-/- n=4-5, Middle-age (MA) WT n=4, MA Rage-/- n=4, Old WT n=5, Old Rage-/- n=6. (B) (Left panel) Representative images of LV sections stained with an anti-Smad2-3 antibody. Bar, 20 µm. (Right panel) Quantification of Smad2/3 signal. Young WT n=5, Young Rage-/- n=5, MA WT n=4, MA Rage-/- n=4, Old WT n=4, Old Rage-/- n=5. (C) (Left panel) Representative images of LV sections stained with an anti-TFGbetaR1 antibody. Bar, 20 µm. (Right panel) Quantification of TFGbetaR1 signal. Young WT n=5, Young Rage-/- n=5, MA WT n=4, MA Rage-/- n=4, Old WT n=4, Old Rage-/- n=5. Each dot represents a mouse; mean ± SD are shown (*, P<0.05; **, P<0.01; ***, P<0.001; 2-way ANOVA plus Bonferroni post-hoc test for multiple comparisons).
    Figure Legend Snippet: RAGE deficiency induces age-associated TGF-β signaling. (A) Relative expression of Tgfb1 gene. Young WT n=4, Young Rage-/- n=4-5, Middle-age (MA) WT n=4, MA Rage-/- n=4, Old WT n=5, Old Rage-/- n=6. (B) (Left panel) Representative images of LV sections stained with an anti-Smad2-3 antibody. Bar, 20 µm. (Right panel) Quantification of Smad2/3 signal. Young WT n=5, Young Rage-/- n=5, MA WT n=4, MA Rage-/- n=4, Old WT n=4, Old Rage-/- n=5. (C) (Left panel) Representative images of LV sections stained with an anti-TFGbetaR1 antibody. Bar, 20 µm. (Right panel) Quantification of TFGbetaR1 signal. Young WT n=5, Young Rage-/- n=5, MA WT n=4, MA Rage-/- n=4, Old WT n=4, Old Rage-/- n=5. Each dot represents a mouse; mean ± SD are shown (*, P<0.05; **, P<0.01; ***, P<0.001; 2-way ANOVA plus Bonferroni post-hoc test for multiple comparisons).

    Techniques Used: Expressing, Staining

    Recombinant sRAGE reduces TGFbetaR1 expression and inhibits Smad2/3 signaling in hcFbs. HcFbs were stimulated with nothing (Ctrl) or the indicated concentrations of sRAGE for 4, 8 or 12 h. TGF-β1 (10 ng/ml) was used as positive control when indicated. (A) TGF-β1 released in the supernatant of cells determined by ELISA; n=6. (B) TFGbetaR1 expression determined by FACS analysis; n=3-8. (C) Quantification of P-Smad2-3 expression determined by FACS analysis 4 h after stimulation; n=3. (D) (Left panel) Representative immunofluorescence images for P-Smad2-3 (green) 4 h after stimulation; nuclei were stained with Hoechst (blue). Bar, 50 μm. (Right panel) Quantification of nuclear P-Smad2-3 expression; n=3 Each dot represents a biological replicate; mean ± SD are shown (*, P<0.05; **, P<0.01; ***, P<0.001; t-test or 1-way ANOVA plus Bonferroni post-hoc test for multiple comparisons between Ctrl and sRAGE at the same time point; dotted line: t-test between Ctrl and TGF-β1).
    Figure Legend Snippet: Recombinant sRAGE reduces TGFbetaR1 expression and inhibits Smad2/3 signaling in hcFbs. HcFbs were stimulated with nothing (Ctrl) or the indicated concentrations of sRAGE for 4, 8 or 12 h. TGF-β1 (10 ng/ml) was used as positive control when indicated. (A) TGF-β1 released in the supernatant of cells determined by ELISA; n=6. (B) TFGbetaR1 expression determined by FACS analysis; n=3-8. (C) Quantification of P-Smad2-3 expression determined by FACS analysis 4 h after stimulation; n=3. (D) (Left panel) Representative immunofluorescence images for P-Smad2-3 (green) 4 h after stimulation; nuclei were stained with Hoechst (blue). Bar, 50 μm. (Right panel) Quantification of nuclear P-Smad2-3 expression; n=3 Each dot represents a biological replicate; mean ± SD are shown (*, P<0.05; **, P<0.01; ***, P<0.001; t-test or 1-way ANOVA plus Bonferroni post-hoc test for multiple comparisons between Ctrl and sRAGE at the same time point; dotted line: t-test between Ctrl and TGF-β1).

    Techniques Used: Recombinant, Expressing, Positive Control, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining

    p smad2 3  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p smad2 3
    RAGE deficiency induces age-associated TGF-β signaling. (A) Relative expression of Tgfb1 gene. Young WT n=4, Young Rage-/- n=4-5, Middle-age (MA) WT n=4, MA Rage-/- n=4, Old WT n=5, Old Rage-/- n=6. (B) (Left panel) Representative images of LV sections stained with an <t>anti-Smad2-3</t> antibody. Bar, 20 µm. (Right panel) Quantification of Smad2/3 signal. Young WT n=5, Young Rage-/- n=5, MA WT n=4, MA Rage-/- n=4, Old WT n=4, Old Rage-/- n=5. (C) (Left panel) Representative images of LV sections stained with an anti-TFGbetaR1 antibody. Bar, 20 µm. (Right panel) Quantification of TFGbetaR1 signal. Young WT n=5, Young Rage-/- n=5, MA WT n=4, MA Rage-/- n=4, Old WT n=4, Old Rage-/- n=5. Each dot represents a mouse; mean ± SD are shown (*, P<0.05; **, P<0.01; ***, P<0.001; 2-way ANOVA plus Bonferroni post-hoc test for multiple comparisons).
    P Smad2 3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Soluble Receptor for Advanced Glycation End-products regulates age-associated Cardiac Fibrosis"

    Article Title: Soluble Receptor for Advanced Glycation End-products regulates age-associated Cardiac Fibrosis

    Journal: International Journal of Biological Sciences

    doi: 10.7150/ijbs.56379

    RAGE deficiency induces age-associated TGF-β signaling. (A) Relative expression of Tgfb1 gene. Young WT n=4, Young Rage-/- n=4-5, Middle-age (MA) WT n=4, MA Rage-/- n=4, Old WT n=5, Old Rage-/- n=6. (B) (Left panel) Representative images of LV sections stained with an anti-Smad2-3 antibody. Bar, 20 µm. (Right panel) Quantification of Smad2/3 signal. Young WT n=5, Young Rage-/- n=5, MA WT n=4, MA Rage-/- n=4, Old WT n=4, Old Rage-/- n=5. (C) (Left panel) Representative images of LV sections stained with an anti-TFGbetaR1 antibody. Bar, 20 µm. (Right panel) Quantification of TFGbetaR1 signal. Young WT n=5, Young Rage-/- n=5, MA WT n=4, MA Rage-/- n=4, Old WT n=4, Old Rage-/- n=5. Each dot represents a mouse; mean ± SD are shown (*, P<0.05; **, P<0.01; ***, P<0.001; 2-way ANOVA plus Bonferroni post-hoc test for multiple comparisons).
    Figure Legend Snippet: RAGE deficiency induces age-associated TGF-β signaling. (A) Relative expression of Tgfb1 gene. Young WT n=4, Young Rage-/- n=4-5, Middle-age (MA) WT n=4, MA Rage-/- n=4, Old WT n=5, Old Rage-/- n=6. (B) (Left panel) Representative images of LV sections stained with an anti-Smad2-3 antibody. Bar, 20 µm. (Right panel) Quantification of Smad2/3 signal. Young WT n=5, Young Rage-/- n=5, MA WT n=4, MA Rage-/- n=4, Old WT n=4, Old Rage-/- n=5. (C) (Left panel) Representative images of LV sections stained with an anti-TFGbetaR1 antibody. Bar, 20 µm. (Right panel) Quantification of TFGbetaR1 signal. Young WT n=5, Young Rage-/- n=5, MA WT n=4, MA Rage-/- n=4, Old WT n=4, Old Rage-/- n=5. Each dot represents a mouse; mean ± SD are shown (*, P<0.05; **, P<0.01; ***, P<0.001; 2-way ANOVA plus Bonferroni post-hoc test for multiple comparisons).

    Techniques Used: Expressing, Staining

    Recombinant sRAGE reduces TGFbetaR1 expression and inhibits Smad2/3 signaling in hcFbs. HcFbs were stimulated with nothing (Ctrl) or the indicated concentrations of sRAGE for 4, 8 or 12 h. TGF-β1 (10 ng/ml) was used as positive control when indicated. (A) TGF-β1 released in the supernatant of cells determined by ELISA; n=6. (B) TFGbetaR1 expression determined by FACS analysis; n=3-8. (C) Quantification of P-Smad2-3 expression determined by FACS analysis 4 h after stimulation; n=3. (D) (Left panel) Representative immunofluorescence images for P-Smad2-3 (green) 4 h after stimulation; nuclei were stained with Hoechst (blue). Bar, 50 μm. (Right panel) Quantification of nuclear P-Smad2-3 expression; n=3 Each dot represents a biological replicate; mean ± SD are shown (*, P<0.05; **, P<0.01; ***, P<0.001; t-test or 1-way ANOVA plus Bonferroni post-hoc test for multiple comparisons between Ctrl and sRAGE at the same time point; dotted line: t-test between Ctrl and TGF-β1).
    Figure Legend Snippet: Recombinant sRAGE reduces TGFbetaR1 expression and inhibits Smad2/3 signaling in hcFbs. HcFbs were stimulated with nothing (Ctrl) or the indicated concentrations of sRAGE for 4, 8 or 12 h. TGF-β1 (10 ng/ml) was used as positive control when indicated. (A) TGF-β1 released in the supernatant of cells determined by ELISA; n=6. (B) TFGbetaR1 expression determined by FACS analysis; n=3-8. (C) Quantification of P-Smad2-3 expression determined by FACS analysis 4 h after stimulation; n=3. (D) (Left panel) Representative immunofluorescence images for P-Smad2-3 (green) 4 h after stimulation; nuclei were stained with Hoechst (blue). Bar, 50 μm. (Right panel) Quantification of nuclear P-Smad2-3 expression; n=3 Each dot represents a biological replicate; mean ± SD are shown (*, P<0.05; **, P<0.01; ***, P<0.001; t-test or 1-way ANOVA plus Bonferroni post-hoc test for multiple comparisons between Ctrl and sRAGE at the same time point; dotted line: t-test between Ctrl and TGF-β1).

    Techniques Used: Recombinant, Expressing, Positive Control, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining

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    Cell lysates prepared from ADSCs treated with TGFβ, bFGF or untreated (Unt) were subjected to SDS-PAGE and immunoblotted. (A) 4-day lysates were probed with anti-α-SMA monoclonal antibody or anti-GAPDH antibody as a loading control. Blot is representative of three independent experiments. (B) Lysates prepared at 1 hour of treatment were immunoblotted with <t>anti-phospho-Smad2</t> (pSmad2) and with total Smad antibody. Blot is representative of three independent experiments. Dash represents 37 kD (A) or 50 kD (B). (C, D) After 4 days of treatment, cells were replated onto collagen-coated glass coverslips for two hours before fixation, permeabilization, and staining with anti-vinculin antibody (C, top), rhodamine-phalloidin (C, bottom), or anti-α-SMA monoclonal antibody (D). Insets in (D) show rhodamine-phalloidin staining of the same fields. All images are representative of three independent experiments. Scale bars = 50 µm.
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    Serelaxin reactivates Rxfp1 expression via histone modifications. (A) Schematic representing the mouse Rxfp1 locus with locations of CHIP-qPCR primers. (B) qPCR analysis showing the enrichment of 4 different histone modification marks (active: H3K4me3 and H3K27ac, repressive: H3K9me3, H3K27me3) in the Rxfp1 promoter region (Amplicon 1-3) and intron 10 (Amplicon 4). The enrichment of TGFβ1-influenced H3K4me3, H3K9me3 and H3K27me3 marks were significantly compromised by Serelaxin if performed with amplicons 1-3 targeting the promoter region but not with amplicon 4 targeting intron10. (C) ChIP-qPCR analysis showing the enrichment of histone modification marks in the Rxfp1 promoter region after RXFP1 knockdown. Upon RXFP1 knockdown, treatment with Serelaxin did not significantly increase the activating modifications or decrease the repressive modification marks. (D) Western blot analysis showing protein levels of <t>pSMAD2</t> and pSMAD3 in sham, AAC-operated and AAC-operated+Serelaxin-treated mouse hearts, total SMAD2 and SMAD3 were used as protein loading controls. AAC-operated hearts showed increased levels of pSMAD2 and pSMAD3 compared to sham. Upon treatment with Serelaxin these protein levels were significantly reduced. (E) qPCR analysis showing the enrichment of <t>pSMAD2/3</t> in the Rxfp1 promoter region (Amplicon 2) and intron 10 (Amplicon 4). The enrichment of TGFβ1-induced pSMAD2/3 was significantly compromised by Serelaxin. The qPCR analysis with primer targeting intron10 did not show any significant differences between these groups. Student t-test was used for single comparison and one-way ANOVA with Bonferroni post-hoc analysis was used for multiple group comparisons. Gene expression and associated error bars, representing mean ± SEM, n≥3, n.s. no significance, ** p<0.01, *** p<0.001, **** p<0.0001.
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    Cell lysates prepared from ADSCs treated with TGFβ, bFGF or untreated (Unt) were subjected to SDS-PAGE and immunoblotted. (A) 4-day lysates were probed with anti-α-SMA monoclonal antibody or anti-GAPDH antibody as a loading control. Blot is representative of three independent experiments. (B) Lysates prepared at 1 hour of treatment were immunoblotted with anti-phospho-Smad2 (pSmad2) and with total Smad antibody. Blot is representative of three independent experiments. Dash represents 37 kD (A) or 50 kD (B). (C, D) After 4 days of treatment, cells were replated onto collagen-coated glass coverslips for two hours before fixation, permeabilization, and staining with anti-vinculin antibody (C, top), rhodamine-phalloidin (C, bottom), or anti-α-SMA monoclonal antibody (D). Insets in (D) show rhodamine-phalloidin staining of the same fields. All images are representative of three independent experiments. Scale bars = 50 µm.

    Journal: PLoS ONE

    Article Title: Reversible Modulation of Myofibroblast Differentiation in Adipose-Derived Mesenchymal Stem Cells

    doi: 10.1371/journal.pone.0086865

    Figure Lengend Snippet: Cell lysates prepared from ADSCs treated with TGFβ, bFGF or untreated (Unt) were subjected to SDS-PAGE and immunoblotted. (A) 4-day lysates were probed with anti-α-SMA monoclonal antibody or anti-GAPDH antibody as a loading control. Blot is representative of three independent experiments. (B) Lysates prepared at 1 hour of treatment were immunoblotted with anti-phospho-Smad2 (pSmad2) and with total Smad antibody. Blot is representative of three independent experiments. Dash represents 37 kD (A) or 50 kD (B). (C, D) After 4 days of treatment, cells were replated onto collagen-coated glass coverslips for two hours before fixation, permeabilization, and staining with anti-vinculin antibody (C, top), rhodamine-phalloidin (C, bottom), or anti-α-SMA monoclonal antibody (D). Insets in (D) show rhodamine-phalloidin staining of the same fields. All images are representative of three independent experiments. Scale bars = 50 µm.

    Article Snippet: Samples containing equal amounts of protein were resolved by SDS-PAGE, transferred to nitrocellulose membranes, and detected using the following antibodies and dilutions: α-SMA Clone 1A4 (Sigma) at 1∶5000, fibronectin HFN7.1 culture supernatant at 1∶5000 (Developmental Studies Hybridoma Bank, Iowa City, Iowa), collagen (pro-) type I (aminopropeptide)-concentrate SP1.D8 (Developmental Studies Hybridoma Bank, Iowa City, Iowa) used at 0.2 µg/mL, phospho-Smad2 (Ser465/467) (Cell Signaling) at 1∶1000, Smad2/3 (Cell Signaling) at 1∶1000, anti-MAP kinase activated (diphosphorylated ERK-1&2) (Sigma) at 1∶10,000, p44/42 MAPK (Erk1/2) (Cell Signaling) at 1∶1000, and GAPDH at 1∶2000 (Cell Signaling).

    Techniques: SDS Page, Staining

    (A) Lysates were harvested for cells grown as indicated in the legend for lanes 1–4, and immunoblotted with anti-phospho Smad2 or anti-total Smad antibody. GAPDH was used as the loading control. Blot is representative of three independent experiments. (B, C) bFGF, TGF-β receptor inhibitor (TGFβ-RI), or DMSO was added to TGF-β-differentiated ADSCs on day 4. Total RNA was isolated at 6, 24, and 48 hours of treatment and qRT-PCR was performed for type I collagen (B) and tenascin-C (C) expression relative to expression in TGF-β-differentiated ADSCs on day 4, using ubiquitin C as the normalization control. Graphs represent the average of multiple samples from three independent experiments +/− SEM. *p<0.05, **p<0.01, and ***p<0.001. The p-values are for comparisons to expression in TGF-β-differentiated ADSCs, unless otherwise indicated.

    Journal: PLoS ONE

    Article Title: Reversible Modulation of Myofibroblast Differentiation in Adipose-Derived Mesenchymal Stem Cells

    doi: 10.1371/journal.pone.0086865

    Figure Lengend Snippet: (A) Lysates were harvested for cells grown as indicated in the legend for lanes 1–4, and immunoblotted with anti-phospho Smad2 or anti-total Smad antibody. GAPDH was used as the loading control. Blot is representative of three independent experiments. (B, C) bFGF, TGF-β receptor inhibitor (TGFβ-RI), or DMSO was added to TGF-β-differentiated ADSCs on day 4. Total RNA was isolated at 6, 24, and 48 hours of treatment and qRT-PCR was performed for type I collagen (B) and tenascin-C (C) expression relative to expression in TGF-β-differentiated ADSCs on day 4, using ubiquitin C as the normalization control. Graphs represent the average of multiple samples from three independent experiments +/− SEM. *p<0.05, **p<0.01, and ***p<0.001. The p-values are for comparisons to expression in TGF-β-differentiated ADSCs, unless otherwise indicated.

    Article Snippet: Samples containing equal amounts of protein were resolved by SDS-PAGE, transferred to nitrocellulose membranes, and detected using the following antibodies and dilutions: α-SMA Clone 1A4 (Sigma) at 1∶5000, fibronectin HFN7.1 culture supernatant at 1∶5000 (Developmental Studies Hybridoma Bank, Iowa City, Iowa), collagen (pro-) type I (aminopropeptide)-concentrate SP1.D8 (Developmental Studies Hybridoma Bank, Iowa City, Iowa) used at 0.2 µg/mL, phospho-Smad2 (Ser465/467) (Cell Signaling) at 1∶1000, Smad2/3 (Cell Signaling) at 1∶1000, anti-MAP kinase activated (diphosphorylated ERK-1&2) (Sigma) at 1∶10,000, p44/42 MAPK (Erk1/2) (Cell Signaling) at 1∶1000, and GAPDH at 1∶2000 (Cell Signaling).

    Techniques: Isolation, Quantitative RT-PCR, Expressing

    (A) The % contraction of fibrin-fibronectin matrices by differentiated and re-differentiated cells was averaged for 6–14 total reactions (+/− SEM) from three independent experiments. **p<0.01, ***p<0.001 (B) A Transwell migration assay was performed with re-differentiated cells. Unt, bFGF, and TGFβ data are from . Quantification represents the average number of cells per field +/− SEM from three to four independent experiments. **p<0.01, ***p<0.001. (C) Comparison of myofibroblast and fibroblast features. TGF-β-differentiated ADSCs are myofibroblastic, contractile, and produce increased type I collagen, fibronectin, α-SMA, and phospho-Smad2. Fibroblast-like cells lack myofibroblastic features, are more migratory, and have increased levels of tenascin-C, vimentin, and phospho-ERK1/2. These fibroblastic and myofibroblastic phenotypes are not terminal and are reversed by switching the respective growth factor treatments.

    Journal: PLoS ONE

    Article Title: Reversible Modulation of Myofibroblast Differentiation in Adipose-Derived Mesenchymal Stem Cells

    doi: 10.1371/journal.pone.0086865

    Figure Lengend Snippet: (A) The % contraction of fibrin-fibronectin matrices by differentiated and re-differentiated cells was averaged for 6–14 total reactions (+/− SEM) from three independent experiments. **p<0.01, ***p<0.001 (B) A Transwell migration assay was performed with re-differentiated cells. Unt, bFGF, and TGFβ data are from . Quantification represents the average number of cells per field +/− SEM from three to four independent experiments. **p<0.01, ***p<0.001. (C) Comparison of myofibroblast and fibroblast features. TGF-β-differentiated ADSCs are myofibroblastic, contractile, and produce increased type I collagen, fibronectin, α-SMA, and phospho-Smad2. Fibroblast-like cells lack myofibroblastic features, are more migratory, and have increased levels of tenascin-C, vimentin, and phospho-ERK1/2. These fibroblastic and myofibroblastic phenotypes are not terminal and are reversed by switching the respective growth factor treatments.

    Article Snippet: Samples containing equal amounts of protein were resolved by SDS-PAGE, transferred to nitrocellulose membranes, and detected using the following antibodies and dilutions: α-SMA Clone 1A4 (Sigma) at 1∶5000, fibronectin HFN7.1 culture supernatant at 1∶5000 (Developmental Studies Hybridoma Bank, Iowa City, Iowa), collagen (pro-) type I (aminopropeptide)-concentrate SP1.D8 (Developmental Studies Hybridoma Bank, Iowa City, Iowa) used at 0.2 µg/mL, phospho-Smad2 (Ser465/467) (Cell Signaling) at 1∶1000, Smad2/3 (Cell Signaling) at 1∶1000, anti-MAP kinase activated (diphosphorylated ERK-1&2) (Sigma) at 1∶10,000, p44/42 MAPK (Erk1/2) (Cell Signaling) at 1∶1000, and GAPDH at 1∶2000 (Cell Signaling).

    Techniques: Transwell Migration Assay

    Serelaxin reactivates Rxfp1 expression via histone modifications. (A) Schematic representing the mouse Rxfp1 locus with locations of CHIP-qPCR primers. (B) qPCR analysis showing the enrichment of 4 different histone modification marks (active: H3K4me3 and H3K27ac, repressive: H3K9me3, H3K27me3) in the Rxfp1 promoter region (Amplicon 1-3) and intron 10 (Amplicon 4). The enrichment of TGFβ1-influenced H3K4me3, H3K9me3 and H3K27me3 marks were significantly compromised by Serelaxin if performed with amplicons 1-3 targeting the promoter region but not with amplicon 4 targeting intron10. (C) ChIP-qPCR analysis showing the enrichment of histone modification marks in the Rxfp1 promoter region after RXFP1 knockdown. Upon RXFP1 knockdown, treatment with Serelaxin did not significantly increase the activating modifications or decrease the repressive modification marks. (D) Western blot analysis showing protein levels of pSMAD2 and pSMAD3 in sham, AAC-operated and AAC-operated+Serelaxin-treated mouse hearts, total SMAD2 and SMAD3 were used as protein loading controls. AAC-operated hearts showed increased levels of pSMAD2 and pSMAD3 compared to sham. Upon treatment with Serelaxin these protein levels were significantly reduced. (E) qPCR analysis showing the enrichment of pSMAD2/3 in the Rxfp1 promoter region (Amplicon 2) and intron 10 (Amplicon 4). The enrichment of TGFβ1-induced pSMAD2/3 was significantly compromised by Serelaxin. The qPCR analysis with primer targeting intron10 did not show any significant differences between these groups. Student t-test was used for single comparison and one-way ANOVA with Bonferroni post-hoc analysis was used for multiple group comparisons. Gene expression and associated error bars, representing mean ± SEM, n≥3, n.s. no significance, ** p<0.01, *** p<0.001, **** p<0.0001.

    Journal: Theranostics

    Article Title: Serelaxin alleviates cardiac fibrosis through inhibiting endothelial-to-mesenchymal transition via RXFP1

    doi: 10.7150/thno.38640

    Figure Lengend Snippet: Serelaxin reactivates Rxfp1 expression via histone modifications. (A) Schematic representing the mouse Rxfp1 locus with locations of CHIP-qPCR primers. (B) qPCR analysis showing the enrichment of 4 different histone modification marks (active: H3K4me3 and H3K27ac, repressive: H3K9me3, H3K27me3) in the Rxfp1 promoter region (Amplicon 1-3) and intron 10 (Amplicon 4). The enrichment of TGFβ1-influenced H3K4me3, H3K9me3 and H3K27me3 marks were significantly compromised by Serelaxin if performed with amplicons 1-3 targeting the promoter region but not with amplicon 4 targeting intron10. (C) ChIP-qPCR analysis showing the enrichment of histone modification marks in the Rxfp1 promoter region after RXFP1 knockdown. Upon RXFP1 knockdown, treatment with Serelaxin did not significantly increase the activating modifications or decrease the repressive modification marks. (D) Western blot analysis showing protein levels of pSMAD2 and pSMAD3 in sham, AAC-operated and AAC-operated+Serelaxin-treated mouse hearts, total SMAD2 and SMAD3 were used as protein loading controls. AAC-operated hearts showed increased levels of pSMAD2 and pSMAD3 compared to sham. Upon treatment with Serelaxin these protein levels were significantly reduced. (E) qPCR analysis showing the enrichment of pSMAD2/3 in the Rxfp1 promoter region (Amplicon 2) and intron 10 (Amplicon 4). The enrichment of TGFβ1-induced pSMAD2/3 was significantly compromised by Serelaxin. The qPCR analysis with primer targeting intron10 did not show any significant differences between these groups. Student t-test was used for single comparison and one-way ANOVA with Bonferroni post-hoc analysis was used for multiple group comparisons. Gene expression and associated error bars, representing mean ± SEM, n≥3, n.s. no significance, ** p<0.01, *** p<0.001, **** p<0.0001.

    Article Snippet: pSMAD2/3 , 1:300 , Cell Signaling , 5678.

    Techniques: Expressing, Modification, Amplification, Western Blot

    Antibodies used in ChIP-qPCR

    Journal: Theranostics

    Article Title: Serelaxin alleviates cardiac fibrosis through inhibiting endothelial-to-mesenchymal transition via RXFP1

    doi: 10.7150/thno.38640

    Figure Lengend Snippet: Antibodies used in ChIP-qPCR

    Article Snippet: pSMAD2/3 , 1:300 , Cell Signaling , 5678.

    Techniques:

    A., and Smad2 and Smad3 mRNA B. ; and TMEPAI mRNA C. in human normal mammary epithelial cells (HMEC) and various triple negative breast cancer cell lines (MDA-MB-231, BT20, HCC1937, MDA-MB-157, Hs578T) along with TMEPAI knockdown MDA-MB-231 cells (231-TMKD/TMKD).

    Journal: Genes & Cancer

    Article Title: Increased Smad3 and reduced Smad2 levels mediate the functional switch of TGF-β from growth suppressor to growth and metastasis promoter through TMEPAI/PMEPA1 in triple negative breast cancer

    doi: 10.18632/genesandcancer.194

    Figure Lengend Snippet: A., and Smad2 and Smad3 mRNA B. ; and TMEPAI mRNA C. in human normal mammary epithelial cells (HMEC) and various triple negative breast cancer cell lines (MDA-MB-231, BT20, HCC1937, MDA-MB-157, Hs578T) along with TMEPAI knockdown MDA-MB-231 cells (231-TMKD/TMKD).

    Article Snippet: Materials: TGF-β (R&D, MN), Antibodies to TMEPAI/PMEPA1 (Abnova, (mouse monoclonal) Taiwan and Proteintech, (rabbit polyclonal) CA), pSmad3 (Rockland, PA), H33258 (Bisbenzimide) and Tubulin (Sigma, MO), GAPDH (R&D, MN), pSmad2, Smad2/3 pAkt, Akt, PTEN, Snail, Slug, p27 and Actin (Cell Signaling, MA).

    Techniques:

    A. Relative levels of Smad2, Smad3, TMEPAI and GAPDH in MDA-MB-231 cells expressing control shRNA, Smad2 shRNA and Smad3 shRNA. B.-E. Growth curves of MDA-MB-231 cells expressing control shRNA (B), Smad2 shRNA (C), Smad3 shRNA (D) and TMEPAI shRNA (E) in the absence or presence of TGF-β (2 ng/ml).

    Journal: Genes & Cancer

    Article Title: Increased Smad3 and reduced Smad2 levels mediate the functional switch of TGF-β from growth suppressor to growth and metastasis promoter through TMEPAI/PMEPA1 in triple negative breast cancer

    doi: 10.18632/genesandcancer.194

    Figure Lengend Snippet: A. Relative levels of Smad2, Smad3, TMEPAI and GAPDH in MDA-MB-231 cells expressing control shRNA, Smad2 shRNA and Smad3 shRNA. B.-E. Growth curves of MDA-MB-231 cells expressing control shRNA (B), Smad2 shRNA (C), Smad3 shRNA (D) and TMEPAI shRNA (E) in the absence or presence of TGF-β (2 ng/ml).

    Article Snippet: Materials: TGF-β (R&D, MN), Antibodies to TMEPAI/PMEPA1 (Abnova, (mouse monoclonal) Taiwan and Proteintech, (rabbit polyclonal) CA), pSmad3 (Rockland, PA), H33258 (Bisbenzimide) and Tubulin (Sigma, MO), GAPDH (R&D, MN), pSmad2, Smad2/3 pAkt, Akt, PTEN, Snail, Slug, p27 and Actin (Cell Signaling, MA).

    Techniques: Expressing, shRNA

    A. Relative expression of phospho Smad2/3, Total Smad2/3 and TMEPAI in MDA-MB-231 cells expressing Con shRNA, Smad2 shRNA and Smad3 shRNA in the absence or presence of TGF-β (2 ng/ml), B. Relative levels of TMEPAI mRNAs in human mammary epithelial cells (HME) and MDA-MB-231 cells that are expressing Con shRNA, TMEPAI shRNA (TMKD), Smad2 shRNA (Smad2KD) or Smad3 shRNA (Smad3KD) in the absence or presence of TGF-β (2 ng/ml), C. 12XCAGA-Luc reporter activity in MDA-MB-231 cells expressing Con ShRNA, Smad2 shRNA, Smad3 shRNA both in the absence or presence of TGF-β (2 ng/ml). D. 3XARE-Luc reporter activity in MDA-MB-231 cells expressing Con ShRNA, Smad2 shRNA, Smad3 shRNA both in the absence or presence of TGF-β (2 ng/ml). E. 12xCAGA-Luc reporter activity in MDA-MB-231 cells expressing Con ShRNA (231_CON) and TMEPAI shRNA (231_TMKD) in the absence or presence of TGF-β (2 ng/ml). F. 3XARE-Luc reporter activity in MDA-MB-231 cells expressing Con ShRNA (231_CON) and TMEPAI shRNA (231_TMKD) in the absence or presence of TGF-β (2 ng/ml). G. Schematic representation of three different size TMEPAI promoters tagged with luciferase reporter (−2251-Luc, −973-Luc, −301-Luc) and corresponding luciferase reporter activities in MDA-MB-231 cells in the absence or presence of TGF-β (2 ng/ml). H. TMEPAI promoter activity in MDA-MB-231 cells expressing con shRNA, Smad2 shRNA, and Smad3 shRNA in the absence or presence of TGF-β (2 ng/ml) using 2251 bp TMEPAI promoter (−2251-Luc).

    Journal: Genes & Cancer

    Article Title: Increased Smad3 and reduced Smad2 levels mediate the functional switch of TGF-β from growth suppressor to growth and metastasis promoter through TMEPAI/PMEPA1 in triple negative breast cancer

    doi: 10.18632/genesandcancer.194

    Figure Lengend Snippet: A. Relative expression of phospho Smad2/3, Total Smad2/3 and TMEPAI in MDA-MB-231 cells expressing Con shRNA, Smad2 shRNA and Smad3 shRNA in the absence or presence of TGF-β (2 ng/ml), B. Relative levels of TMEPAI mRNAs in human mammary epithelial cells (HME) and MDA-MB-231 cells that are expressing Con shRNA, TMEPAI shRNA (TMKD), Smad2 shRNA (Smad2KD) or Smad3 shRNA (Smad3KD) in the absence or presence of TGF-β (2 ng/ml), C. 12XCAGA-Luc reporter activity in MDA-MB-231 cells expressing Con ShRNA, Smad2 shRNA, Smad3 shRNA both in the absence or presence of TGF-β (2 ng/ml). D. 3XARE-Luc reporter activity in MDA-MB-231 cells expressing Con ShRNA, Smad2 shRNA, Smad3 shRNA both in the absence or presence of TGF-β (2 ng/ml). E. 12xCAGA-Luc reporter activity in MDA-MB-231 cells expressing Con ShRNA (231_CON) and TMEPAI shRNA (231_TMKD) in the absence or presence of TGF-β (2 ng/ml). F. 3XARE-Luc reporter activity in MDA-MB-231 cells expressing Con ShRNA (231_CON) and TMEPAI shRNA (231_TMKD) in the absence or presence of TGF-β (2 ng/ml). G. Schematic representation of three different size TMEPAI promoters tagged with luciferase reporter (−2251-Luc, −973-Luc, −301-Luc) and corresponding luciferase reporter activities in MDA-MB-231 cells in the absence or presence of TGF-β (2 ng/ml). H. TMEPAI promoter activity in MDA-MB-231 cells expressing con shRNA, Smad2 shRNA, and Smad3 shRNA in the absence or presence of TGF-β (2 ng/ml) using 2251 bp TMEPAI promoter (−2251-Luc).

    Article Snippet: Materials: TGF-β (R&D, MN), Antibodies to TMEPAI/PMEPA1 (Abnova, (mouse monoclonal) Taiwan and Proteintech, (rabbit polyclonal) CA), pSmad3 (Rockland, PA), H33258 (Bisbenzimide) and Tubulin (Sigma, MO), GAPDH (R&D, MN), pSmad2, Smad2/3 pAkt, Akt, PTEN, Snail, Slug, p27 and Actin (Cell Signaling, MA).

    Techniques: Expressing, shRNA, Activity Assay, Luciferase

    A. Growth curves of MDA-MB-231 cells expressing control shRNA (CON shRNA), Smad2 shRNA, Smad3 shRNA or Smad3shRNA along with human TMEPAI cDNA (Smad3 shRNA+hTM) in the absence or presence of TGF-β (2 ng/ml). B. Relative expression of phosphorylated Akt (pAkt), Smad2, Smad3, Snail, Slug, PTEN, p27 and TMEPAI in MDA-MB-231 cells expressing Con shRNA (CON), Smad2 shRNA (S2KD), Smad3 shRNA (S3KD) and Smad3 shRNA along with human TMEPAI cDNA (S3KD+hTM) in the absence or presence of TGF-β (2 ng/ml). Phase contrast images of toluidine blue stained transit well invasion assay (C) and relative invasion index (D) of MDA-MB-231 cells expressing control shRNA (CON shRNA), Smad2 shRNA, Smad3 shRNA and Smad3shRNA along with human TMEPAI cDNA in the absence or presence of TGF-β (2 ng/ml).

    Journal: Genes & Cancer

    Article Title: Increased Smad3 and reduced Smad2 levels mediate the functional switch of TGF-β from growth suppressor to growth and metastasis promoter through TMEPAI/PMEPA1 in triple negative breast cancer

    doi: 10.18632/genesandcancer.194

    Figure Lengend Snippet: A. Growth curves of MDA-MB-231 cells expressing control shRNA (CON shRNA), Smad2 shRNA, Smad3 shRNA or Smad3shRNA along with human TMEPAI cDNA (Smad3 shRNA+hTM) in the absence or presence of TGF-β (2 ng/ml). B. Relative expression of phosphorylated Akt (pAkt), Smad2, Smad3, Snail, Slug, PTEN, p27 and TMEPAI in MDA-MB-231 cells expressing Con shRNA (CON), Smad2 shRNA (S2KD), Smad3 shRNA (S3KD) and Smad3 shRNA along with human TMEPAI cDNA (S3KD+hTM) in the absence or presence of TGF-β (2 ng/ml). Phase contrast images of toluidine blue stained transit well invasion assay (C) and relative invasion index (D) of MDA-MB-231 cells expressing control shRNA (CON shRNA), Smad2 shRNA, Smad3 shRNA and Smad3shRNA along with human TMEPAI cDNA in the absence or presence of TGF-β (2 ng/ml).

    Article Snippet: Materials: TGF-β (R&D, MN), Antibodies to TMEPAI/PMEPA1 (Abnova, (mouse monoclonal) Taiwan and Proteintech, (rabbit polyclonal) CA), pSmad3 (Rockland, PA), H33258 (Bisbenzimide) and Tubulin (Sigma, MO), GAPDH (R&D, MN), pSmad2, Smad2/3 pAkt, Akt, PTEN, Snail, Slug, p27 and Actin (Cell Signaling, MA).

    Techniques: Expressing, shRNA, Staining, Invasion Assay

    Relative mRNA expression of Smad2 A. , Smad3 B. , TMEPAI C. , Snai1 D. , Slug E. in MDA-MB-231 (231) cells that are expressing control, TMEPAI (TMKD), Smad2 (Smad2KD) and Smad3 (Smad3KD) shRNAs in the absence or presence of TGF-β (2 ng/ml) relative to normal human mammary epithelial cells (HMEC).

    Journal: Genes & Cancer

    Article Title: Increased Smad3 and reduced Smad2 levels mediate the functional switch of TGF-β from growth suppressor to growth and metastasis promoter through TMEPAI/PMEPA1 in triple negative breast cancer

    doi: 10.18632/genesandcancer.194

    Figure Lengend Snippet: Relative mRNA expression of Smad2 A. , Smad3 B. , TMEPAI C. , Snai1 D. , Slug E. in MDA-MB-231 (231) cells that are expressing control, TMEPAI (TMKD), Smad2 (Smad2KD) and Smad3 (Smad3KD) shRNAs in the absence or presence of TGF-β (2 ng/ml) relative to normal human mammary epithelial cells (HMEC).

    Article Snippet: Materials: TGF-β (R&D, MN), Antibodies to TMEPAI/PMEPA1 (Abnova, (mouse monoclonal) Taiwan and Proteintech, (rabbit polyclonal) CA), pSmad3 (Rockland, PA), H33258 (Bisbenzimide) and Tubulin (Sigma, MO), GAPDH (R&D, MN), pSmad2, Smad2/3 pAkt, Akt, PTEN, Snail, Slug, p27 and Actin (Cell Signaling, MA).

    Techniques: Expressing

    A. Relative expression of Smad2, Smad3 and TMEPAI in Control (HCC), Smad2 knockdown (S2KD) and Smad3 knockdown (S3KD) HCC1937 TNBC cells. B. Growth of control HCC1937 (HCC) in the presence and absence of TGF-β. C. Growth of Smad2 knockdown HCC1937 (S2KD) in the presence and absence of TGF-β. D. Growth of Smad3 knockdown HCC1937 (S3KD) in the presence and absence of TGF-β. E. Relative expressions of E-Cad, Snail and Slug in control (CON) and TMEPAI knockdown (TMKD) HCC1937 cells. F. Relative expressions of E-Cad and Vimentin in control (CON), Smad2 knockdown (S2KD) and Smad3 knockdown (S3KD) HCC1937 cells.

    Journal: Genes & Cancer

    Article Title: Increased Smad3 and reduced Smad2 levels mediate the functional switch of TGF-β from growth suppressor to growth and metastasis promoter through TMEPAI/PMEPA1 in triple negative breast cancer

    doi: 10.18632/genesandcancer.194

    Figure Lengend Snippet: A. Relative expression of Smad2, Smad3 and TMEPAI in Control (HCC), Smad2 knockdown (S2KD) and Smad3 knockdown (S3KD) HCC1937 TNBC cells. B. Growth of control HCC1937 (HCC) in the presence and absence of TGF-β. C. Growth of Smad2 knockdown HCC1937 (S2KD) in the presence and absence of TGF-β. D. Growth of Smad3 knockdown HCC1937 (S3KD) in the presence and absence of TGF-β. E. Relative expressions of E-Cad, Snail and Slug in control (CON) and TMEPAI knockdown (TMKD) HCC1937 cells. F. Relative expressions of E-Cad and Vimentin in control (CON), Smad2 knockdown (S2KD) and Smad3 knockdown (S3KD) HCC1937 cells.

    Article Snippet: Materials: TGF-β (R&D, MN), Antibodies to TMEPAI/PMEPA1 (Abnova, (mouse monoclonal) Taiwan and Proteintech, (rabbit polyclonal) CA), pSmad3 (Rockland, PA), H33258 (Bisbenzimide) and Tubulin (Sigma, MO), GAPDH (R&D, MN), pSmad2, Smad2/3 pAkt, Akt, PTEN, Snail, Slug, p27 and Actin (Cell Signaling, MA).

    Techniques: Expressing

    Kaplan Meier curves for overall survival of triple negative breast cancer patients in relation to expression of TMEPAI/PMEPA1 (A), Smad2 (B), Smad3 (C) or Smad4 (D) mRNA using a publicly accessible database (GSE58812). E. Western blots of TMEPAI and total Smad2/3 proteins in primary tumors from human breast cancer patients (BC1- BC5) and corresponding normal/benign (N1-N4) samples relative to MDA-MB-231 cells (231).

    Journal: Genes & Cancer

    Article Title: Increased Smad3 and reduced Smad2 levels mediate the functional switch of TGF-β from growth suppressor to growth and metastasis promoter through TMEPAI/PMEPA1 in triple negative breast cancer

    doi: 10.18632/genesandcancer.194

    Figure Lengend Snippet: Kaplan Meier curves for overall survival of triple negative breast cancer patients in relation to expression of TMEPAI/PMEPA1 (A), Smad2 (B), Smad3 (C) or Smad4 (D) mRNA using a publicly accessible database (GSE58812). E. Western blots of TMEPAI and total Smad2/3 proteins in primary tumors from human breast cancer patients (BC1- BC5) and corresponding normal/benign (N1-N4) samples relative to MDA-MB-231 cells (231).

    Article Snippet: Materials: TGF-β (R&D, MN), Antibodies to TMEPAI/PMEPA1 (Abnova, (mouse monoclonal) Taiwan and Proteintech, (rabbit polyclonal) CA), pSmad3 (Rockland, PA), H33258 (Bisbenzimide) and Tubulin (Sigma, MO), GAPDH (R&D, MN), pSmad2, Smad2/3 pAkt, Akt, PTEN, Snail, Slug, p27 and Actin (Cell Signaling, MA).

    Techniques: Expressing, Western Blot

    The data demonstrate that the consequences of switch from Smad2 to Smad3 signaling pathway results in converting TGF-β from tumor suppressor to pro-oncogene as cells acquire increasing malignant properties through Smad3 mediated TMEPAI expression.

    Journal: Genes & Cancer

    Article Title: Increased Smad3 and reduced Smad2 levels mediate the functional switch of TGF-β from growth suppressor to growth and metastasis promoter through TMEPAI/PMEPA1 in triple negative breast cancer

    doi: 10.18632/genesandcancer.194

    Figure Lengend Snippet: The data demonstrate that the consequences of switch from Smad2 to Smad3 signaling pathway results in converting TGF-β from tumor suppressor to pro-oncogene as cells acquire increasing malignant properties through Smad3 mediated TMEPAI expression.

    Article Snippet: Materials: TGF-β (R&D, MN), Antibodies to TMEPAI/PMEPA1 (Abnova, (mouse monoclonal) Taiwan and Proteintech, (rabbit polyclonal) CA), pSmad3 (Rockland, PA), H33258 (Bisbenzimide) and Tubulin (Sigma, MO), GAPDH (R&D, MN), pSmad2, Smad2/3 pAkt, Akt, PTEN, Snail, Slug, p27 and Actin (Cell Signaling, MA).

    Techniques: Expressing

    PCI34051 alleviates cardiac fibrosis in transverse aortic constriction (TAC) mice through the TGF- β 1-Smad2/3 pathway. (a, b) Picrosirius red staining of mouse cardiac tissues; representative images and quantification are shown. Scale bar = 50 μ m. The expression levels of the fibrosis marker genes Col1a1 (c), Fn1 (d), Acta2 (e), and Tgfb1 (f) were determined using quantitative real-time polymerase chain reaction ( n = 5–6 per group). (g) The cardiac expression levels of Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 were analyzed using western blotting. Actb was used as a loading control. Representative blots are shown. (h–k) Quantification of Fn1, Acta2, Tgfb1, and p-Smad2/3 to Smad2/3 ( n = 5–6 per group).

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Hdac8 Inhibitor Alleviates Transverse Aortic Constriction-Induced Heart Failure in Mice by Downregulating Ace1

    doi: 10.1155/2022/6227330

    Figure Lengend Snippet: PCI34051 alleviates cardiac fibrosis in transverse aortic constriction (TAC) mice through the TGF- β 1-Smad2/3 pathway. (a, b) Picrosirius red staining of mouse cardiac tissues; representative images and quantification are shown. Scale bar = 50 μ m. The expression levels of the fibrosis marker genes Col1a1 (c), Fn1 (d), Acta2 (e), and Tgfb1 (f) were determined using quantitative real-time polymerase chain reaction ( n = 5–6 per group). (g) The cardiac expression levels of Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 were analyzed using western blotting. Actb was used as a loading control. Representative blots are shown. (h–k) Quantification of Fn1, Acta2, Tgfb1, and p-Smad2/3 to Smad2/3 ( n = 5–6 per group).

    Article Snippet: Anti-phospho-Smad2/3 (8828), anti-Smad2/3 (3102), anti-Rela (8242), and anti-Nfkbia (4812) antibodies were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Staining, Expressing, Marker, Real-time Polymerase Chain Reaction, Western Blot

    PCI34051 alleviates pulmonary congestion and fibrosis in transverse aortic constriction (TAC) mice. (a) The ratio of lung weight-to-bodyweight (LW/BW) in the sham+vehicle, sham+PCI34051 (10 mg/kg bodyweight/day), TAC+vehicle, and TAC+PCI34051 (3, 10, or 30 mg/kg bodyweight/day) groups ( n = 5–6 per group) was determined. Representative images of mouse lungs (B). (b) Representative images of pulmonary tissues stained with hematoxylin and eosin. Scale bar = 50 μ m. (c) Representative images of pulmonary tissues stained with Picrosirius red. Scale bar = 50 μ m. (d) Pulmonary fibrosis was quantified using ImageJ software. (e–h) The mRNA levels of Col1a1 , Fn1 , Acta2 , and Tgfb1 were evaluated using quantitative real-time polymerase chain reaction ( n = 5–6 per group). (i–m) Representative western blots and quantification of Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 levels in the pulmonary tissues ( n = 5–6 per group).

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Hdac8 Inhibitor Alleviates Transverse Aortic Constriction-Induced Heart Failure in Mice by Downregulating Ace1

    doi: 10.1155/2022/6227330

    Figure Lengend Snippet: PCI34051 alleviates pulmonary congestion and fibrosis in transverse aortic constriction (TAC) mice. (a) The ratio of lung weight-to-bodyweight (LW/BW) in the sham+vehicle, sham+PCI34051 (10 mg/kg bodyweight/day), TAC+vehicle, and TAC+PCI34051 (3, 10, or 30 mg/kg bodyweight/day) groups ( n = 5–6 per group) was determined. Representative images of mouse lungs (B). (b) Representative images of pulmonary tissues stained with hematoxylin and eosin. Scale bar = 50 μ m. (c) Representative images of pulmonary tissues stained with Picrosirius red. Scale bar = 50 μ m. (d) Pulmonary fibrosis was quantified using ImageJ software. (e–h) The mRNA levels of Col1a1 , Fn1 , Acta2 , and Tgfb1 were evaluated using quantitative real-time polymerase chain reaction ( n = 5–6 per group). (i–m) Representative western blots and quantification of Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 levels in the pulmonary tissues ( n = 5–6 per group).

    Article Snippet: Anti-phospho-Smad2/3 (8828), anti-Smad2/3 (3102), anti-Rela (8242), and anti-Nfkbia (4812) antibodies were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Staining, Software, Real-time Polymerase Chain Reaction, Western Blot

    PCI34051 or Hdac8 knockdown mitigates TGF- β 1-induced fibrosis in rat cardiac fibroblasts. (a–e) Rat cardiac fibroblasts were pre-treated with TGF– β 1 (10 ng/mL) for 1 h and cultured in the presence of vehicle or PCI34051 (10 μ M) for 8 h. mRNA levels of Hdac8 , Col1a1 , Fn1 , Acta2 , and Tgfb1 were evaluated using quantitative real-time polymerase chain reaction (qRT-PCR) ( n = 4–6 per group). (f–k) Representative immunoblots and quantification of Hdac8, Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 levels in rat cardiac fibroblasts ( n = 6 per group). Actb was used as a loading control. (l–p) Rat cardiac fibroblasts were transfected with control or short-interfering RNA against Hdac8 and treated with TGF- β 1 (10 ng/mL) for 9 h. The mRNA levels of Hdac8 , Fn1 , Acta2 , Tgfb1 , and Ace1 were determined using qRT-PCR ( n = 5 per group). (q–w) Representative immunoblots and quantification of Hdac8, Ace1, Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 levels in rat cardiac fibroblasts ( n = 4 per group). Actb was used as a loading control.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Hdac8 Inhibitor Alleviates Transverse Aortic Constriction-Induced Heart Failure in Mice by Downregulating Ace1

    doi: 10.1155/2022/6227330

    Figure Lengend Snippet: PCI34051 or Hdac8 knockdown mitigates TGF- β 1-induced fibrosis in rat cardiac fibroblasts. (a–e) Rat cardiac fibroblasts were pre-treated with TGF– β 1 (10 ng/mL) for 1 h and cultured in the presence of vehicle or PCI34051 (10 μ M) for 8 h. mRNA levels of Hdac8 , Col1a1 , Fn1 , Acta2 , and Tgfb1 were evaluated using quantitative real-time polymerase chain reaction (qRT-PCR) ( n = 4–6 per group). (f–k) Representative immunoblots and quantification of Hdac8, Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 levels in rat cardiac fibroblasts ( n = 6 per group). Actb was used as a loading control. (l–p) Rat cardiac fibroblasts were transfected with control or short-interfering RNA against Hdac8 and treated with TGF- β 1 (10 ng/mL) for 9 h. The mRNA levels of Hdac8 , Fn1 , Acta2 , Tgfb1 , and Ace1 were determined using qRT-PCR ( n = 5 per group). (q–w) Representative immunoblots and quantification of Hdac8, Ace1, Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 levels in rat cardiac fibroblasts ( n = 4 per group). Actb was used as a loading control.

    Article Snippet: Anti-phospho-Smad2/3 (8828), anti-Smad2/3 (3102), anti-Rela (8242), and anti-Nfkbia (4812) antibodies were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Cell Culture, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Western Blot, Transfection, Small Interfering RNA

    Suppression of HDAC8 attenuates fibrosis, inflammation, cardiac dysfunction, and pulmonary congestion in heart failure. Schematic diagram depicting the Hdac8 selective inhibitor- (PCI34051-) mediated or Hdac8 short-interfering RNA-mediated inhibition of transverse aortic constriction- (TAC-) induced heart failure. TAC-mediated pressure overload upregulates the expression of Hdac8 and Ace1 and downregulates the expression of Ace2 in the heart and lungs. In cardiomyocytes, overexpression of Hdac8 upregulates the expression of Ace1 and downregulates the expression of Ace2. PCI34051 treatment or Hdac8 knockdown mitigates TGF- β 1-induced upregulation of p-Smad2/3, Col1a1, Fn1, and Acta2 in vitro. PCI34051 regulates the TNF α -mediated or Ace1 overexpression-mediated expression of Rela and Nfkbia. PCI34051 alleviates cardiac hypertrophy and dysfunction, inflammation, fibrosis, and pulmonary congestion in heart failure.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Hdac8 Inhibitor Alleviates Transverse Aortic Constriction-Induced Heart Failure in Mice by Downregulating Ace1

    doi: 10.1155/2022/6227330

    Figure Lengend Snippet: Suppression of HDAC8 attenuates fibrosis, inflammation, cardiac dysfunction, and pulmonary congestion in heart failure. Schematic diagram depicting the Hdac8 selective inhibitor- (PCI34051-) mediated or Hdac8 short-interfering RNA-mediated inhibition of transverse aortic constriction- (TAC-) induced heart failure. TAC-mediated pressure overload upregulates the expression of Hdac8 and Ace1 and downregulates the expression of Ace2 in the heart and lungs. In cardiomyocytes, overexpression of Hdac8 upregulates the expression of Ace1 and downregulates the expression of Ace2. PCI34051 treatment or Hdac8 knockdown mitigates TGF- β 1-induced upregulation of p-Smad2/3, Col1a1, Fn1, and Acta2 in vitro. PCI34051 regulates the TNF α -mediated or Ace1 overexpression-mediated expression of Rela and Nfkbia. PCI34051 alleviates cardiac hypertrophy and dysfunction, inflammation, fibrosis, and pulmonary congestion in heart failure.

    Article Snippet: Anti-phospho-Smad2/3 (8828), anti-Smad2/3 (3102), anti-Rela (8242), and anti-Nfkbia (4812) antibodies were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Small Interfering RNA, Inhibition, Expressing, Over Expression, In Vitro

    RAGE deficiency induces age-associated TGF-β signaling. (A) Relative expression of Tgfb1 gene. Young WT n=4, Young Rage-/- n=4-5, Middle-age (MA) WT n=4, MA Rage-/- n=4, Old WT n=5, Old Rage-/- n=6. (B) (Left panel) Representative images of LV sections stained with an anti-Smad2-3 antibody. Bar, 20 µm. (Right panel) Quantification of Smad2/3 signal. Young WT n=5, Young Rage-/- n=5, MA WT n=4, MA Rage-/- n=4, Old WT n=4, Old Rage-/- n=5. (C) (Left panel) Representative images of LV sections stained with an anti-TFGbetaR1 antibody. Bar, 20 µm. (Right panel) Quantification of TFGbetaR1 signal. Young WT n=5, Young Rage-/- n=5, MA WT n=4, MA Rage-/- n=4, Old WT n=4, Old Rage-/- n=5. Each dot represents a mouse; mean ± SD are shown (*, P<0.05; **, P<0.01; ***, P<0.001; 2-way ANOVA plus Bonferroni post-hoc test for multiple comparisons).

    Journal: International Journal of Biological Sciences

    Article Title: Soluble Receptor for Advanced Glycation End-products regulates age-associated Cardiac Fibrosis

    doi: 10.7150/ijbs.56379

    Figure Lengend Snippet: RAGE deficiency induces age-associated TGF-β signaling. (A) Relative expression of Tgfb1 gene. Young WT n=4, Young Rage-/- n=4-5, Middle-age (MA) WT n=4, MA Rage-/- n=4, Old WT n=5, Old Rage-/- n=6. (B) (Left panel) Representative images of LV sections stained with an anti-Smad2-3 antibody. Bar, 20 µm. (Right panel) Quantification of Smad2/3 signal. Young WT n=5, Young Rage-/- n=5, MA WT n=4, MA Rage-/- n=4, Old WT n=4, Old Rage-/- n=5. (C) (Left panel) Representative images of LV sections stained with an anti-TFGbetaR1 antibody. Bar, 20 µm. (Right panel) Quantification of TFGbetaR1 signal. Young WT n=5, Young Rage-/- n=5, MA WT n=4, MA Rage-/- n=4, Old WT n=4, Old Rage-/- n=5. Each dot represents a mouse; mean ± SD are shown (*, P<0.05; **, P<0.01; ***, P<0.001; 2-way ANOVA plus Bonferroni post-hoc test for multiple comparisons).

    Article Snippet: One hundred thousand cells were collected, washed with PBS, fixed and permeabilized with BD Cytofix/Cytoperm™ fixation/permeabilization Kit (#554714, BD Bioscience) and stained with primary antibodies for TGFbetaR1 (1 µg/10 6 cells, ABF17-I, Sigma-Aldrich) and P-Smad2-3 (1:800, #8828, Cell Signaling Technology) for 30 minutes at rt.

    Techniques: Expressing, Staining

    Recombinant sRAGE reduces TGFbetaR1 expression and inhibits Smad2/3 signaling in hcFbs. HcFbs were stimulated with nothing (Ctrl) or the indicated concentrations of sRAGE for 4, 8 or 12 h. TGF-β1 (10 ng/ml) was used as positive control when indicated. (A) TGF-β1 released in the supernatant of cells determined by ELISA; n=6. (B) TFGbetaR1 expression determined by FACS analysis; n=3-8. (C) Quantification of P-Smad2-3 expression determined by FACS analysis 4 h after stimulation; n=3. (D) (Left panel) Representative immunofluorescence images for P-Smad2-3 (green) 4 h after stimulation; nuclei were stained with Hoechst (blue). Bar, 50 μm. (Right panel) Quantification of nuclear P-Smad2-3 expression; n=3 Each dot represents a biological replicate; mean ± SD are shown (*, P<0.05; **, P<0.01; ***, P<0.001; t-test or 1-way ANOVA plus Bonferroni post-hoc test for multiple comparisons between Ctrl and sRAGE at the same time point; dotted line: t-test between Ctrl and TGF-β1).

    Journal: International Journal of Biological Sciences

    Article Title: Soluble Receptor for Advanced Glycation End-products regulates age-associated Cardiac Fibrosis

    doi: 10.7150/ijbs.56379

    Figure Lengend Snippet: Recombinant sRAGE reduces TGFbetaR1 expression and inhibits Smad2/3 signaling in hcFbs. HcFbs were stimulated with nothing (Ctrl) or the indicated concentrations of sRAGE for 4, 8 or 12 h. TGF-β1 (10 ng/ml) was used as positive control when indicated. (A) TGF-β1 released in the supernatant of cells determined by ELISA; n=6. (B) TFGbetaR1 expression determined by FACS analysis; n=3-8. (C) Quantification of P-Smad2-3 expression determined by FACS analysis 4 h after stimulation; n=3. (D) (Left panel) Representative immunofluorescence images for P-Smad2-3 (green) 4 h after stimulation; nuclei were stained with Hoechst (blue). Bar, 50 μm. (Right panel) Quantification of nuclear P-Smad2-3 expression; n=3 Each dot represents a biological replicate; mean ± SD are shown (*, P<0.05; **, P<0.01; ***, P<0.001; t-test or 1-way ANOVA plus Bonferroni post-hoc test for multiple comparisons between Ctrl and sRAGE at the same time point; dotted line: t-test between Ctrl and TGF-β1).

    Article Snippet: One hundred thousand cells were collected, washed with PBS, fixed and permeabilized with BD Cytofix/Cytoperm™ fixation/permeabilization Kit (#554714, BD Bioscience) and stained with primary antibodies for TGFbetaR1 (1 µg/10 6 cells, ABF17-I, Sigma-Aldrich) and P-Smad2-3 (1:800, #8828, Cell Signaling Technology) for 30 minutes at rt.

    Techniques: Recombinant, Expressing, Positive Control, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining