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mouse anti sma  (Boster Bio)


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    Boster Bio mouse anti sma
    FIGURE 1. Dlk1 was readily induced and remains elevated during chronic liver injury. A, Western blot analysis of Dlk1 expression in CCl4-injured livers at different time points. Densitometric quantifications related to -actin were analyzed (n 5). B, Dlk1 mRNA in injured livers (CCl4 injury for 4 weeks) was detected by in situ hybridization. Tissue sections were counterstained with hematoxylin. Scale bars, 50 m. C, co-localization of Dlk1 (red) and <t>-SMA</t> (green) in HSCs by <t>dual</t> <t>immunofluorescence</t> staining. Nuclei were counterstained with DAPI (blue). Scale bars, 20 m. D, HSCs and hepatocytes were isolated from injured livers and Dlk1 expression was detected by RT-PCR.
    Mouse Anti Sma, supplied by Boster Bio, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse anti sma/product/Boster Bio
    Average 86 stars, based on 1 article reviews
    mouse anti sma - by Bioz Stars, 2026-02
    86/100 stars

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    1) Product Images from "Delta-like 1 Serves as a New Target and Contributor to Liver Fibrosis Down-regulated by Mesenchymal Stem Cell Transplantation"

    Article Title: Delta-like 1 Serves as a New Target and Contributor to Liver Fibrosis Down-regulated by Mesenchymal Stem Cell Transplantation

    Journal: Journal of Biological Chemistry

    doi: 10.1074/jbc.m110.194498

    FIGURE 1. Dlk1 was readily induced and remains elevated during chronic liver injury. A, Western blot analysis of Dlk1 expression in CCl4-injured livers at different time points. Densitometric quantifications related to -actin were analyzed (n 5). B, Dlk1 mRNA in injured livers (CCl4 injury for 4 weeks) was detected by in situ hybridization. Tissue sections were counterstained with hematoxylin. Scale bars, 50 m. C, co-localization of Dlk1 (red) and -SMA (green) in HSCs by dual immunofluorescence staining. Nuclei were counterstained with DAPI (blue). Scale bars, 20 m. D, HSCs and hepatocytes were isolated from injured livers and Dlk1 expression was detected by RT-PCR.
    Figure Legend Snippet: FIGURE 1. Dlk1 was readily induced and remains elevated during chronic liver injury. A, Western blot analysis of Dlk1 expression in CCl4-injured livers at different time points. Densitometric quantifications related to -actin were analyzed (n 5). B, Dlk1 mRNA in injured livers (CCl4 injury for 4 weeks) was detected by in situ hybridization. Tissue sections were counterstained with hematoxylin. Scale bars, 50 m. C, co-localization of Dlk1 (red) and -SMA (green) in HSCs by dual immunofluorescence staining. Nuclei were counterstained with DAPI (blue). Scale bars, 20 m. D, HSCs and hepatocytes were isolated from injured livers and Dlk1 expression was detected by RT-PCR.

    Techniques Used: Western Blot, Expressing, In Situ Hybridization, Immunofluorescence, Staining, Isolation, Reverse Transcription Polymerase Chain Reaction

    FIGURE 2. Large form of Dlk1, rather than the small one, facilitated HSC activation in vitro. A, RT-PCR analysis of gene expression in HSCs freshly isolated andinducedwithnormalculturedHEK293medium(Control),thesmallformofDlk1(S),andthelargeone(L)for7days.PPAR,peroxisomeproliferator-activated receptor. B, -SMA and col I(1) mRNA levels related to -actin in HSCs treated for 7 days were examined by real time PCR (*, p 0.05 versus control, n 5). C, lipid droplet observation and immunofluorescence staining of -SMA in HSCs for 7 and 14 days (D) of treatment. Nuclei were visualized by staining with DAPI (blue). Arrows indicate the lipid droplets. Scale bars, 100 m. D, cell fluorescence intensities of immunofluorescence staining of -SMA were analyzed by LSM 5 Image Examiner (**, p 0.01 versus control, n 10).
    Figure Legend Snippet: FIGURE 2. Large form of Dlk1, rather than the small one, facilitated HSC activation in vitro. A, RT-PCR analysis of gene expression in HSCs freshly isolated andinducedwithnormalculturedHEK293medium(Control),thesmallformofDlk1(S),andthelargeone(L)for7days.PPAR,peroxisomeproliferator-activated receptor. B, -SMA and col I(1) mRNA levels related to -actin in HSCs treated for 7 days were examined by real time PCR (*, p 0.05 versus control, n 5). C, lipid droplet observation and immunofluorescence staining of -SMA in HSCs for 7 and 14 days (D) of treatment. Nuclei were visualized by staining with DAPI (blue). Arrows indicate the lipid droplets. Scale bars, 100 m. D, cell fluorescence intensities of immunofluorescence staining of -SMA were analyzed by LSM 5 Image Examiner (**, p 0.01 versus control, n 10).

    Techniques Used: Activation Assay, In Vitro, Reverse Transcription Polymerase Chain Reaction, Gene Expression, Isolation, Control, Real-time Polymerase Chain Reaction, Immunofluorescence, Staining, Fluorescence

    FIGURE 3. Dlk1 participated in HSC activation and liver fibrosis in vivo. A, Dlk1 mRNA levels in CCl4-injured mice, and injured animals with PBS and synthetic siRNA administration (**, p 0.01 versus values in CCl4 injured group, n 5). B and C, expressions of -SMA and col I(1) in injured livers after siRNA and Dlk1-L administration were examined by real time PCR. Medium from normal cultured HEK293 was used as controls (*, p 0.05; **, p 0.01, versus values in CCl4-injured group, n 5). D, Sirius Red staining for fibrosis in the groups described above. The degree of liver fibrosis was semi-quantified by measuring the relative area of fibrosis using computer software. Results are presented in the right histogram (*, p 0.05; **, p 0.01, versus values in CCl4-injured group, n 5). Scale bars, 50 m.
    Figure Legend Snippet: FIGURE 3. Dlk1 participated in HSC activation and liver fibrosis in vivo. A, Dlk1 mRNA levels in CCl4-injured mice, and injured animals with PBS and synthetic siRNA administration (**, p 0.01 versus values in CCl4 injured group, n 5). B and C, expressions of -SMA and col I(1) in injured livers after siRNA and Dlk1-L administration were examined by real time PCR. Medium from normal cultured HEK293 was used as controls (*, p 0.05; **, p 0.01, versus values in CCl4-injured group, n 5). D, Sirius Red staining for fibrosis in the groups described above. The degree of liver fibrosis was semi-quantified by measuring the relative area of fibrosis using computer software. Results are presented in the right histogram (*, p 0.05; **, p 0.01, versus values in CCl4-injured group, n 5). Scale bars, 50 m.

    Techniques Used: Activation Assay, In Vivo, Real-time Polymerase Chain Reaction, Cell Culture, Staining, Software

    FIGURE 4. BM-MSC transplantation attenuated CCl4-induced HSC activation and liver fibrosis. A, Sirius Red staining for fibrosis. A, panel i, normal group; panel ii, CCl4-injured group; panel iii, PBS group; panel iv, BM-MSC-transplanted group. Scale bars, 50 m. B, score of the liver fibrosis. The degree of liver fibrosis was semi-quantified by measuring the relative areas of fibrosis using computer software (*, p 0.05 versus values in CCl4-injured group, n 6). C, immuno- fluorescence staining of -SMA (green) in the experimental livers. C, panel i, normal group; panel ii, CCl4-injured group; panel iii, PBS group; panel iv, BM-MSC- transplanted group. Nuclei were counterstained with DAPI (blue). Arrows indicate the -SMA positive cells. Scale bars, 20 m. D, -SMA and col I(1) mRNA expression related to -actin in the experimental livers were examined by real time PCR (*, p 0.05 versus values in CCl4-injured group, n 5).
    Figure Legend Snippet: FIGURE 4. BM-MSC transplantation attenuated CCl4-induced HSC activation and liver fibrosis. A, Sirius Red staining for fibrosis. A, panel i, normal group; panel ii, CCl4-injured group; panel iii, PBS group; panel iv, BM-MSC-transplanted group. Scale bars, 50 m. B, score of the liver fibrosis. The degree of liver fibrosis was semi-quantified by measuring the relative areas of fibrosis using computer software (*, p 0.05 versus values in CCl4-injured group, n 6). C, immuno- fluorescence staining of -SMA (green) in the experimental livers. C, panel i, normal group; panel ii, CCl4-injured group; panel iii, PBS group; panel iv, BM-MSC- transplanted group. Nuclei were counterstained with DAPI (blue). Arrows indicate the -SMA positive cells. Scale bars, 20 m. D, -SMA and col I(1) mRNA expression related to -actin in the experimental livers were examined by real time PCR (*, p 0.05 versus values in CCl4-injured group, n 5).

    Techniques Used: Transplantation Assay, Activation Assay, Staining, Software, Fluorescence, Expressing, Real-time Polymerase Chain Reaction

    FIGURE 5. Transplanted BM-MSCs inhibited HSC activation by modulating Dlk1 expression. A, Dlk1 mRNA levels in experimental livers examined by real time PCR (*, p 0.01 versus values in CCl4-injured group, n 5). B, in situ hybridization analysis of Dlk1 mRNA in experimental liver tissues. B, panel i, normal group; panel ii, CCl4-injured group; panel iii, PBS group; panel iv, BM-MSC-transplanted group. Tissue sections were counterstained with hematoxylin. Arrows indicate Dlk1-positive hepatocytes. Scale bars, 50 m. C, co-localization of Dlk1 (red) and -SMA (green) in HSCs by dual immunofluorescence staining. Nuclei were counterstained with DAPI (blue). Arrows indicate cells co-localized with Dlk1 and -SMA. Scale bars, 20 m. D, -SMA and col I(1) mRNA levels in experimental livers after additional administration with different amounts of Dlk1-L were detected by real time PCR (*, p 0.05; **, p 0.01, n 5).
    Figure Legend Snippet: FIGURE 5. Transplanted BM-MSCs inhibited HSC activation by modulating Dlk1 expression. A, Dlk1 mRNA levels in experimental livers examined by real time PCR (*, p 0.01 versus values in CCl4-injured group, n 5). B, in situ hybridization analysis of Dlk1 mRNA in experimental liver tissues. B, panel i, normal group; panel ii, CCl4-injured group; panel iii, PBS group; panel iv, BM-MSC-transplanted group. Tissue sections were counterstained with hematoxylin. Arrows indicate Dlk1-positive hepatocytes. Scale bars, 50 m. C, co-localization of Dlk1 (red) and -SMA (green) in HSCs by dual immunofluorescence staining. Nuclei were counterstained with DAPI (blue). Arrows indicate cells co-localized with Dlk1 and -SMA. Scale bars, 20 m. D, -SMA and col I(1) mRNA levels in experimental livers after additional administration with different amounts of Dlk1-L were detected by real time PCR (*, p 0.05; **, p 0.01, n 5).

    Techniques Used: Activation Assay, Expressing, Real-time Polymerase Chain Reaction, In Situ Hybridization, Immunofluorescence, Staining

    FIGURE 7. Recombinant FGF2 could inhibit Dlk1 expression, HSC activation, and liver fibrosis. A, analysis of Dlk1 expression in hepatocytes by real time PCR. Hepatocytes from injured livers were exposed to 20 ng/ml FGF2 in vitro for 72 h (*, p 0.05 versus values in normal cultured injured hepatocytes, n 5). B,Dlk1mRNAlevelsininjuredliversafteradministrationofFGF2(50g/kgbodyweight)invivo(**,p0.01versusvaluesinCCl4-injuredgroup,n5).C,-SMA andcolI(1)mRNAlevelsintheexperimentalliverswereexaminedbyrealtimePCR(**,p0.01versusvaluesinCCl4injuredgroup,n5).D,SiriusRedstaining shows the extent of fibrosis in the experimental livers. The degree of liver fibrosis was semi-quantified by measuring the relative area of fibrosis using computer software. Results are presented in the right histogram (**, p 0.01 versus values in CCl4-injured group, n 5). Scale bars, 50 m.
    Figure Legend Snippet: FIGURE 7. Recombinant FGF2 could inhibit Dlk1 expression, HSC activation, and liver fibrosis. A, analysis of Dlk1 expression in hepatocytes by real time PCR. Hepatocytes from injured livers were exposed to 20 ng/ml FGF2 in vitro for 72 h (*, p 0.05 versus values in normal cultured injured hepatocytes, n 5). B,Dlk1mRNAlevelsininjuredliversafteradministrationofFGF2(50g/kgbodyweight)invivo(**,p0.01versusvaluesinCCl4-injuredgroup,n5).C,-SMA andcolI(1)mRNAlevelsintheexperimentalliverswereexaminedbyrealtimePCR(**,p0.01versusvaluesinCCl4injuredgroup,n5).D,SiriusRedstaining shows the extent of fibrosis in the experimental livers. The degree of liver fibrosis was semi-quantified by measuring the relative area of fibrosis using computer software. Results are presented in the right histogram (**, p 0.01 versus values in CCl4-injured group, n 5). Scale bars, 50 m.

    Techniques Used: Recombinant, Expressing, Activation Assay, Real-time Polymerase Chain Reaction, In Vitro, Cell Culture, Software



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    mouse anti sma  (Boster Bio)
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    Boster Bio mouse anti sma
    FIGURE 1. Dlk1 was readily induced and remains elevated during chronic liver injury. A, Western blot analysis of Dlk1 expression in CCl4-injured livers at different time points. Densitometric quantifications related to -actin were analyzed (n 5). B, Dlk1 mRNA in injured livers (CCl4 injury for 4 weeks) was detected by in situ hybridization. Tissue sections were counterstained with hematoxylin. Scale bars, 50 m. C, co-localization of Dlk1 (red) and <t>-SMA</t> (green) in HSCs by <t>dual</t> <t>immunofluorescence</t> staining. Nuclei were counterstained with DAPI (blue). Scale bars, 20 m. D, HSCs and hepatocytes were isolated from injured livers and Dlk1 expression was detected by RT-PCR.
    Mouse Anti Sma, supplied by Boster Bio, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse anti sma/product/Boster Bio
    Average 86 stars, based on 1 article reviews
    mouse anti sma - by Bioz Stars, 2026-02
    86/100 stars
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    FIGURE 1. Dlk1 was readily induced and remains elevated during chronic liver injury. A, Western blot analysis of Dlk1 expression in CCl4-injured livers at different time points. Densitometric quantifications related to -actin were analyzed (n 5). B, Dlk1 mRNA in injured livers (CCl4 injury for 4 weeks) was detected by in situ hybridization. Tissue sections were counterstained with hematoxylin. Scale bars, 50 m. C, co-localization of Dlk1 (red) and -SMA (green) in HSCs by dual immunofluorescence staining. Nuclei were counterstained with DAPI (blue). Scale bars, 20 m. D, HSCs and hepatocytes were isolated from injured livers and Dlk1 expression was detected by RT-PCR.

    Journal: Journal of Biological Chemistry

    Article Title: Delta-like 1 Serves as a New Target and Contributor to Liver Fibrosis Down-regulated by Mesenchymal Stem Cell Transplantation

    doi: 10.1074/jbc.m110.194498

    Figure Lengend Snippet: FIGURE 1. Dlk1 was readily induced and remains elevated during chronic liver injury. A, Western blot analysis of Dlk1 expression in CCl4-injured livers at different time points. Densitometric quantifications related to -actin were analyzed (n 5). B, Dlk1 mRNA in injured livers (CCl4 injury for 4 weeks) was detected by in situ hybridization. Tissue sections were counterstained with hematoxylin. Scale bars, 50 m. C, co-localization of Dlk1 (red) and -SMA (green) in HSCs by dual immunofluorescence staining. Nuclei were counterstained with DAPI (blue). Scale bars, 20 m. D, HSCs and hepatocytes were isolated from injured livers and Dlk1 expression was detected by RT-PCR.

    Article Snippet: Immunofluorescence Staining—Tissue sections were deparaffinized and incubated with mouse anti- -SMA (Boster, China) and goat anti-Dlk1 antibodies (Santa Cruz Biotechnology) for dual immunofluorescence staining as described previously(23), with some modifications.

    Techniques: Western Blot, Expressing, In Situ Hybridization, Immunofluorescence, Staining, Isolation, Reverse Transcription Polymerase Chain Reaction

    FIGURE 2. Large form of Dlk1, rather than the small one, facilitated HSC activation in vitro. A, RT-PCR analysis of gene expression in HSCs freshly isolated andinducedwithnormalculturedHEK293medium(Control),thesmallformofDlk1(S),andthelargeone(L)for7days.PPAR,peroxisomeproliferator-activated receptor. B, -SMA and col I(1) mRNA levels related to -actin in HSCs treated for 7 days were examined by real time PCR (*, p 0.05 versus control, n 5). C, lipid droplet observation and immunofluorescence staining of -SMA in HSCs for 7 and 14 days (D) of treatment. Nuclei were visualized by staining with DAPI (blue). Arrows indicate the lipid droplets. Scale bars, 100 m. D, cell fluorescence intensities of immunofluorescence staining of -SMA were analyzed by LSM 5 Image Examiner (**, p 0.01 versus control, n 10).

    Journal: Journal of Biological Chemistry

    Article Title: Delta-like 1 Serves as a New Target and Contributor to Liver Fibrosis Down-regulated by Mesenchymal Stem Cell Transplantation

    doi: 10.1074/jbc.m110.194498

    Figure Lengend Snippet: FIGURE 2. Large form of Dlk1, rather than the small one, facilitated HSC activation in vitro. A, RT-PCR analysis of gene expression in HSCs freshly isolated andinducedwithnormalculturedHEK293medium(Control),thesmallformofDlk1(S),andthelargeone(L)for7days.PPAR,peroxisomeproliferator-activated receptor. B, -SMA and col I(1) mRNA levels related to -actin in HSCs treated for 7 days were examined by real time PCR (*, p 0.05 versus control, n 5). C, lipid droplet observation and immunofluorescence staining of -SMA in HSCs for 7 and 14 days (D) of treatment. Nuclei were visualized by staining with DAPI (blue). Arrows indicate the lipid droplets. Scale bars, 100 m. D, cell fluorescence intensities of immunofluorescence staining of -SMA were analyzed by LSM 5 Image Examiner (**, p 0.01 versus control, n 10).

    Article Snippet: Immunofluorescence Staining—Tissue sections were deparaffinized and incubated with mouse anti- -SMA (Boster, China) and goat anti-Dlk1 antibodies (Santa Cruz Biotechnology) for dual immunofluorescence staining as described previously(23), with some modifications.

    Techniques: Activation Assay, In Vitro, Reverse Transcription Polymerase Chain Reaction, Gene Expression, Isolation, Control, Real-time Polymerase Chain Reaction, Immunofluorescence, Staining, Fluorescence

    FIGURE 3. Dlk1 participated in HSC activation and liver fibrosis in vivo. A, Dlk1 mRNA levels in CCl4-injured mice, and injured animals with PBS and synthetic siRNA administration (**, p 0.01 versus values in CCl4 injured group, n 5). B and C, expressions of -SMA and col I(1) in injured livers after siRNA and Dlk1-L administration were examined by real time PCR. Medium from normal cultured HEK293 was used as controls (*, p 0.05; **, p 0.01, versus values in CCl4-injured group, n 5). D, Sirius Red staining for fibrosis in the groups described above. The degree of liver fibrosis was semi-quantified by measuring the relative area of fibrosis using computer software. Results are presented in the right histogram (*, p 0.05; **, p 0.01, versus values in CCl4-injured group, n 5). Scale bars, 50 m.

    Journal: Journal of Biological Chemistry

    Article Title: Delta-like 1 Serves as a New Target and Contributor to Liver Fibrosis Down-regulated by Mesenchymal Stem Cell Transplantation

    doi: 10.1074/jbc.m110.194498

    Figure Lengend Snippet: FIGURE 3. Dlk1 participated in HSC activation and liver fibrosis in vivo. A, Dlk1 mRNA levels in CCl4-injured mice, and injured animals with PBS and synthetic siRNA administration (**, p 0.01 versus values in CCl4 injured group, n 5). B and C, expressions of -SMA and col I(1) in injured livers after siRNA and Dlk1-L administration were examined by real time PCR. Medium from normal cultured HEK293 was used as controls (*, p 0.05; **, p 0.01, versus values in CCl4-injured group, n 5). D, Sirius Red staining for fibrosis in the groups described above. The degree of liver fibrosis was semi-quantified by measuring the relative area of fibrosis using computer software. Results are presented in the right histogram (*, p 0.05; **, p 0.01, versus values in CCl4-injured group, n 5). Scale bars, 50 m.

    Article Snippet: Immunofluorescence Staining—Tissue sections were deparaffinized and incubated with mouse anti- -SMA (Boster, China) and goat anti-Dlk1 antibodies (Santa Cruz Biotechnology) for dual immunofluorescence staining as described previously(23), with some modifications.

    Techniques: Activation Assay, In Vivo, Real-time Polymerase Chain Reaction, Cell Culture, Staining, Software

    FIGURE 4. BM-MSC transplantation attenuated CCl4-induced HSC activation and liver fibrosis. A, Sirius Red staining for fibrosis. A, panel i, normal group; panel ii, CCl4-injured group; panel iii, PBS group; panel iv, BM-MSC-transplanted group. Scale bars, 50 m. B, score of the liver fibrosis. The degree of liver fibrosis was semi-quantified by measuring the relative areas of fibrosis using computer software (*, p 0.05 versus values in CCl4-injured group, n 6). C, immuno- fluorescence staining of -SMA (green) in the experimental livers. C, panel i, normal group; panel ii, CCl4-injured group; panel iii, PBS group; panel iv, BM-MSC- transplanted group. Nuclei were counterstained with DAPI (blue). Arrows indicate the -SMA positive cells. Scale bars, 20 m. D, -SMA and col I(1) mRNA expression related to -actin in the experimental livers were examined by real time PCR (*, p 0.05 versus values in CCl4-injured group, n 5).

    Journal: Journal of Biological Chemistry

    Article Title: Delta-like 1 Serves as a New Target and Contributor to Liver Fibrosis Down-regulated by Mesenchymal Stem Cell Transplantation

    doi: 10.1074/jbc.m110.194498

    Figure Lengend Snippet: FIGURE 4. BM-MSC transplantation attenuated CCl4-induced HSC activation and liver fibrosis. A, Sirius Red staining for fibrosis. A, panel i, normal group; panel ii, CCl4-injured group; panel iii, PBS group; panel iv, BM-MSC-transplanted group. Scale bars, 50 m. B, score of the liver fibrosis. The degree of liver fibrosis was semi-quantified by measuring the relative areas of fibrosis using computer software (*, p 0.05 versus values in CCl4-injured group, n 6). C, immuno- fluorescence staining of -SMA (green) in the experimental livers. C, panel i, normal group; panel ii, CCl4-injured group; panel iii, PBS group; panel iv, BM-MSC- transplanted group. Nuclei were counterstained with DAPI (blue). Arrows indicate the -SMA positive cells. Scale bars, 20 m. D, -SMA and col I(1) mRNA expression related to -actin in the experimental livers were examined by real time PCR (*, p 0.05 versus values in CCl4-injured group, n 5).

    Article Snippet: Immunofluorescence Staining—Tissue sections were deparaffinized and incubated with mouse anti- -SMA (Boster, China) and goat anti-Dlk1 antibodies (Santa Cruz Biotechnology) for dual immunofluorescence staining as described previously(23), with some modifications.

    Techniques: Transplantation Assay, Activation Assay, Staining, Software, Fluorescence, Expressing, Real-time Polymerase Chain Reaction

    FIGURE 5. Transplanted BM-MSCs inhibited HSC activation by modulating Dlk1 expression. A, Dlk1 mRNA levels in experimental livers examined by real time PCR (*, p 0.01 versus values in CCl4-injured group, n 5). B, in situ hybridization analysis of Dlk1 mRNA in experimental liver tissues. B, panel i, normal group; panel ii, CCl4-injured group; panel iii, PBS group; panel iv, BM-MSC-transplanted group. Tissue sections were counterstained with hematoxylin. Arrows indicate Dlk1-positive hepatocytes. Scale bars, 50 m. C, co-localization of Dlk1 (red) and -SMA (green) in HSCs by dual immunofluorescence staining. Nuclei were counterstained with DAPI (blue). Arrows indicate cells co-localized with Dlk1 and -SMA. Scale bars, 20 m. D, -SMA and col I(1) mRNA levels in experimental livers after additional administration with different amounts of Dlk1-L were detected by real time PCR (*, p 0.05; **, p 0.01, n 5).

    Journal: Journal of Biological Chemistry

    Article Title: Delta-like 1 Serves as a New Target and Contributor to Liver Fibrosis Down-regulated by Mesenchymal Stem Cell Transplantation

    doi: 10.1074/jbc.m110.194498

    Figure Lengend Snippet: FIGURE 5. Transplanted BM-MSCs inhibited HSC activation by modulating Dlk1 expression. A, Dlk1 mRNA levels in experimental livers examined by real time PCR (*, p 0.01 versus values in CCl4-injured group, n 5). B, in situ hybridization analysis of Dlk1 mRNA in experimental liver tissues. B, panel i, normal group; panel ii, CCl4-injured group; panel iii, PBS group; panel iv, BM-MSC-transplanted group. Tissue sections were counterstained with hematoxylin. Arrows indicate Dlk1-positive hepatocytes. Scale bars, 50 m. C, co-localization of Dlk1 (red) and -SMA (green) in HSCs by dual immunofluorescence staining. Nuclei were counterstained with DAPI (blue). Arrows indicate cells co-localized with Dlk1 and -SMA. Scale bars, 20 m. D, -SMA and col I(1) mRNA levels in experimental livers after additional administration with different amounts of Dlk1-L were detected by real time PCR (*, p 0.05; **, p 0.01, n 5).

    Article Snippet: Immunofluorescence Staining—Tissue sections were deparaffinized and incubated with mouse anti- -SMA (Boster, China) and goat anti-Dlk1 antibodies (Santa Cruz Biotechnology) for dual immunofluorescence staining as described previously(23), with some modifications.

    Techniques: Activation Assay, Expressing, Real-time Polymerase Chain Reaction, In Situ Hybridization, Immunofluorescence, Staining

    FIGURE 7. Recombinant FGF2 could inhibit Dlk1 expression, HSC activation, and liver fibrosis. A, analysis of Dlk1 expression in hepatocytes by real time PCR. Hepatocytes from injured livers were exposed to 20 ng/ml FGF2 in vitro for 72 h (*, p 0.05 versus values in normal cultured injured hepatocytes, n 5). B,Dlk1mRNAlevelsininjuredliversafteradministrationofFGF2(50g/kgbodyweight)invivo(**,p0.01versusvaluesinCCl4-injuredgroup,n5).C,-SMA andcolI(1)mRNAlevelsintheexperimentalliverswereexaminedbyrealtimePCR(**,p0.01versusvaluesinCCl4injuredgroup,n5).D,SiriusRedstaining shows the extent of fibrosis in the experimental livers. The degree of liver fibrosis was semi-quantified by measuring the relative area of fibrosis using computer software. Results are presented in the right histogram (**, p 0.01 versus values in CCl4-injured group, n 5). Scale bars, 50 m.

    Journal: Journal of Biological Chemistry

    Article Title: Delta-like 1 Serves as a New Target and Contributor to Liver Fibrosis Down-regulated by Mesenchymal Stem Cell Transplantation

    doi: 10.1074/jbc.m110.194498

    Figure Lengend Snippet: FIGURE 7. Recombinant FGF2 could inhibit Dlk1 expression, HSC activation, and liver fibrosis. A, analysis of Dlk1 expression in hepatocytes by real time PCR. Hepatocytes from injured livers were exposed to 20 ng/ml FGF2 in vitro for 72 h (*, p 0.05 versus values in normal cultured injured hepatocytes, n 5). B,Dlk1mRNAlevelsininjuredliversafteradministrationofFGF2(50g/kgbodyweight)invivo(**,p0.01versusvaluesinCCl4-injuredgroup,n5).C,-SMA andcolI(1)mRNAlevelsintheexperimentalliverswereexaminedbyrealtimePCR(**,p0.01versusvaluesinCCl4injuredgroup,n5).D,SiriusRedstaining shows the extent of fibrosis in the experimental livers. The degree of liver fibrosis was semi-quantified by measuring the relative area of fibrosis using computer software. Results are presented in the right histogram (**, p 0.01 versus values in CCl4-injured group, n 5). Scale bars, 50 m.

    Article Snippet: Immunofluorescence Staining—Tissue sections were deparaffinized and incubated with mouse anti- -SMA (Boster, China) and goat anti-Dlk1 antibodies (Santa Cruz Biotechnology) for dual immunofluorescence staining as described previously(23), with some modifications.

    Techniques: Recombinant, Expressing, Activation Assay, Real-time Polymerase Chain Reaction, In Vitro, Cell Culture, Software