recombinant rat ngf  (Alomone Labs)


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    Structured Review

    Alomone Labs recombinant rat ngf
    <t>TGF-β1</t> promoted the mRNA expression of <t>NGF</t> in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P
    Recombinant Rat Ngf, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/recombinant rat ngf/product/Alomone Labs
    Average 93 stars, based on 4 article reviews
    Price from $9.99 to $1999.99
    recombinant rat ngf - by Bioz Stars, 2022-09
    93/100 stars

    Images

    1) Product Images from "IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals"

    Article Title: IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals

    Journal: International Journal of Molecular Medicine

    doi: 10.3892/ijmm_2018.3714

    TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P
    Figure Legend Snippet: TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Standard Deviation

    IL-1β and TNF-α suppressed the TGF-β1-induced mRNA expression of NGF in SCDC2 cells by abrogating Smad2/3 and p38 MAPK activities. The effects of IL-1β and TNF-α on TGF-β1-induced mRNA expression of NGF in SCDC2 cells were evaluated using RT-qPCR. The cells were treated with or without (A) IL-1β alone or (B) TNF-α alone at indicated concentrations, (C) TGF-β1 (10 ng/ml) and/or IL-1β (10 ng/ml), and (D) TGF-β1 (10 ng/ml) and/or TNF-α (10 ng/ml). Data represent the mean ± standard deviation (n=6). * P
    Figure Legend Snippet: IL-1β and TNF-α suppressed the TGF-β1-induced mRNA expression of NGF in SCDC2 cells by abrogating Smad2/3 and p38 MAPK activities. The effects of IL-1β and TNF-α on TGF-β1-induced mRNA expression of NGF in SCDC2 cells were evaluated using RT-qPCR. The cells were treated with or without (A) IL-1β alone or (B) TNF-α alone at indicated concentrations, (C) TGF-β1 (10 ng/ml) and/or IL-1β (10 ng/ml), and (D) TGF-β1 (10 ng/ml) and/or TNF-α (10 ng/ml). Data represent the mean ± standard deviation (n=6). * P

    Techniques Used: Expressing, Quantitative RT-PCR, Standard Deviation

    TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells in Smad2/3-dependent and p38 MAPK-dependent manners. Effects of (A) SIS3 (10 µ M), and (B) SB203580 (10 µ M) on expression of NGF mRNA were evaluated as described in Materials and methods. Data represent the mean ± standard deviation (n=6). * P
    Figure Legend Snippet: TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells in Smad2/3-dependent and p38 MAPK-dependent manners. Effects of (A) SIS3 (10 µ M), and (B) SB203580 (10 µ M) on expression of NGF mRNA were evaluated as described in Materials and methods. Data represent the mean ± standard deviation (n=6). * P

    Techniques Used: Expressing, Standard Deviation

    2) Product Images from "IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals"

    Article Title: IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals

    Journal: International Journal of Molecular Medicine

    doi: 10.3892/ijmm_2018.3714

    TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P
    Figure Legend Snippet: TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Standard Deviation

    IL-1β and TNF-α suppressed the TGF-β1-induced mRNA expression of NGF in SCDC2 cells by abrogating Smad2/3 and p38 MAPK activities. The effects of IL-1β and TNF-α on TGF-β1-induced mRNA expression of NGF in SCDC2 cells were evaluated using RT-qPCR. The cells were treated with or without (A) IL-1β alone or (B) TNF-α alone at indicated concentrations, (C) TGF-β1 (10 ng/ml) and/or IL-1β (10 ng/ml), and (D) TGF-β1 (10 ng/ml) and/or TNF-α (10 ng/ml). Data represent the mean ± standard deviation (n=6). * P
    Figure Legend Snippet: IL-1β and TNF-α suppressed the TGF-β1-induced mRNA expression of NGF in SCDC2 cells by abrogating Smad2/3 and p38 MAPK activities. The effects of IL-1β and TNF-α on TGF-β1-induced mRNA expression of NGF in SCDC2 cells were evaluated using RT-qPCR. The cells were treated with or without (A) IL-1β alone or (B) TNF-α alone at indicated concentrations, (C) TGF-β1 (10 ng/ml) and/or IL-1β (10 ng/ml), and (D) TGF-β1 (10 ng/ml) and/or TNF-α (10 ng/ml). Data represent the mean ± standard deviation (n=6). * P

    Techniques Used: Expressing, Quantitative RT-PCR, Standard Deviation

    Nerve growth factor secreted by SCDC2 cells following TGF-β1 stimulation promoted neurite extension from the surface of ATPγS-treated PC12 cells. (A) Neurite extension of PC12 cells was visualized by immunostaining (×200 magnification; scale bar, 50 µ m) with anti-neurofilament H antibody (red) and nuclei were stained with DAPI (blue). SCDC2 cells (2×10 4 cells) and rat pheochromocytoma cells PC12 (1×10 4 cells) were co-cultured and treated with or without TGF-β1 (10 ng/ml) for 4 days. Cells were also treated with TGF-β type I receptor inhibitor SB-431542 (10 µ M), TrkA inhibitor GW441756 (2 nM), IL-1β (10 ng/ml), or TNF-α (10 ng/ml) from the beginning of the co-culture. In addition, ATPγS (100 µ M) was added to all cultures during cell seeding. Dimethyl sulfoxide was added to cell cultures as a vehicle control for SB-431542 and GW441756, respectively. (B) Statistical assessment of neurite extension in PC12 cells co-cultured with SCDC2 cells. Data represent the mean ± standard deviation (n=8). * P
    Figure Legend Snippet: Nerve growth factor secreted by SCDC2 cells following TGF-β1 stimulation promoted neurite extension from the surface of ATPγS-treated PC12 cells. (A) Neurite extension of PC12 cells was visualized by immunostaining (×200 magnification; scale bar, 50 µ m) with anti-neurofilament H antibody (red) and nuclei were stained with DAPI (blue). SCDC2 cells (2×10 4 cells) and rat pheochromocytoma cells PC12 (1×10 4 cells) were co-cultured and treated with or without TGF-β1 (10 ng/ml) for 4 days. Cells were also treated with TGF-β type I receptor inhibitor SB-431542 (10 µ M), TrkA inhibitor GW441756 (2 nM), IL-1β (10 ng/ml), or TNF-α (10 ng/ml) from the beginning of the co-culture. In addition, ATPγS (100 µ M) was added to all cultures during cell seeding. Dimethyl sulfoxide was added to cell cultures as a vehicle control for SB-431542 and GW441756, respectively. (B) Statistical assessment of neurite extension in PC12 cells co-cultured with SCDC2 cells. Data represent the mean ± standard deviation (n=8). * P

    Techniques Used: Immunostaining, Staining, Cell Culture, Co-Culture Assay, Standard Deviation

    Nerve growth factor secreted by SCDC2 cells subsequent to TGF-β1 stimulation promoted the expression of TH mRNA in PC12 cells. SCDC2 cells (7×10 4 cells) and rat pheochromocytoma cells PC12 cells (3.5×10 4 cells) were co-cultured and stimulated with or without TGF-β1 (10 ng/ml) for 24 h. The relative expression level of TH was evaluated using reverse transcription-quantitative polymerase chain reaction in cells also treated with (A) ATPγS (100 µ M), and with (B) TGF-β type I receptor inhibitor SB-431542 (10 µ M), TrkA inhibitor GW441756 (2 nM), IL-1β (10 ng/ml) or TNF-α (10 ng/ml) during the co-culture. Dimethyl sulfoxide was added to cell cultures as a vehicle control for SB-431542 and GW441756, respectively. Data represent the mean ± standard deviation (n=6). * P
    Figure Legend Snippet: Nerve growth factor secreted by SCDC2 cells subsequent to TGF-β1 stimulation promoted the expression of TH mRNA in PC12 cells. SCDC2 cells (7×10 4 cells) and rat pheochromocytoma cells PC12 cells (3.5×10 4 cells) were co-cultured and stimulated with or without TGF-β1 (10 ng/ml) for 24 h. The relative expression level of TH was evaluated using reverse transcription-quantitative polymerase chain reaction in cells also treated with (A) ATPγS (100 µ M), and with (B) TGF-β type I receptor inhibitor SB-431542 (10 µ M), TrkA inhibitor GW441756 (2 nM), IL-1β (10 ng/ml) or TNF-α (10 ng/ml) during the co-culture. Dimethyl sulfoxide was added to cell cultures as a vehicle control for SB-431542 and GW441756, respectively. Data represent the mean ± standard deviation (n=6). * P

    Techniques Used: Expressing, Cell Culture, Real-time Polymerase Chain Reaction, Co-Culture Assay, Standard Deviation

    TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells in Smad2/3-dependent and p38 MAPK-dependent manners. Effects of (A) SIS3 (10 µ M), and (B) SB203580 (10 µ M) on expression of NGF mRNA were evaluated as described in Materials and methods. Data represent the mean ± standard deviation (n=6). * P
    Figure Legend Snippet: TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells in Smad2/3-dependent and p38 MAPK-dependent manners. Effects of (A) SIS3 (10 µ M), and (B) SB203580 (10 µ M) on expression of NGF mRNA were evaluated as described in Materials and methods. Data represent the mean ± standard deviation (n=6). * P

    Techniques Used: Expressing, Standard Deviation

    3) Product Images from "IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals"

    Article Title: IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals

    Journal: International Journal of Molecular Medicine

    doi: 10.3892/ijmm_2018.3714

    TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P
    Figure Legend Snippet: TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P

    Techniques Used: Expressing, Real-time Polymerase Chain Reaction, Standard Deviation

    IL-1β and TNF-α suppressed the TGF-β1-induced mRNA expression of NGF in SCDC2 cells by abrogating Smad2/3 and p38 MAPK activities. The effects of IL-1β and TNF-α on TGF-β1-induced mRNA expression of NGF in SCDC2 cells were evaluated using RT-qPCR. The cells were treated with or without (A) IL-1β alone or (B) TNF-α alone at indicated concentrations, (C) TGF-β1 (10 ng/ml) and/or IL-1β (10 ng/ml), and (D) TGF-β1 (10 ng/ml) and/or TNF-α (10 ng/ml). Data represent the mean ± standard deviation (n=6). * P
    Figure Legend Snippet: IL-1β and TNF-α suppressed the TGF-β1-induced mRNA expression of NGF in SCDC2 cells by abrogating Smad2/3 and p38 MAPK activities. The effects of IL-1β and TNF-α on TGF-β1-induced mRNA expression of NGF in SCDC2 cells were evaluated using RT-qPCR. The cells were treated with or without (A) IL-1β alone or (B) TNF-α alone at indicated concentrations, (C) TGF-β1 (10 ng/ml) and/or IL-1β (10 ng/ml), and (D) TGF-β1 (10 ng/ml) and/or TNF-α (10 ng/ml). Data represent the mean ± standard deviation (n=6). * P

    Techniques Used: Expressing, Quantitative RT-PCR, Standard Deviation

    Nerve growth factor secreted by SCDC2 cells following TGF-β1 stimulation promoted neurite extension from the surface of ATPγS-treated PC12 cells. (A) Neurite extension of PC12 cells was visualized by immunostaining (×200 magnification; scale bar, 50 µ m) with anti-neurofilament H antibody (red) and nuclei were stained with DAPI (blue). SCDC2 cells (2×10 4 cells) and rat pheochromocytoma cells PC12 (1×10 4 cells) were co-cultured and treated with or without TGF-β1 (10 ng/ml) for 4 days. Cells were also treated with TGF-β type I receptor inhibitor SB-431542 (10 µ M), TrkA inhibitor GW441756 (2 nM), IL-1β (10 ng/ml), or TNF-α (10 ng/ml) from the beginning of the co-culture. In addition, ATPγS (100 µ M) was added to all cultures during cell seeding. Dimethyl sulfoxide was added to cell cultures as a vehicle control for SB-431542 and GW441756, respectively. (B) Statistical assessment of neurite extension in PC12 cells co-cultured with SCDC2 cells. Data represent the mean ± standard deviation (n=8). * P
    Figure Legend Snippet: Nerve growth factor secreted by SCDC2 cells following TGF-β1 stimulation promoted neurite extension from the surface of ATPγS-treated PC12 cells. (A) Neurite extension of PC12 cells was visualized by immunostaining (×200 magnification; scale bar, 50 µ m) with anti-neurofilament H antibody (red) and nuclei were stained with DAPI (blue). SCDC2 cells (2×10 4 cells) and rat pheochromocytoma cells PC12 (1×10 4 cells) were co-cultured and treated with or without TGF-β1 (10 ng/ml) for 4 days. Cells were also treated with TGF-β type I receptor inhibitor SB-431542 (10 µ M), TrkA inhibitor GW441756 (2 nM), IL-1β (10 ng/ml), or TNF-α (10 ng/ml) from the beginning of the co-culture. In addition, ATPγS (100 µ M) was added to all cultures during cell seeding. Dimethyl sulfoxide was added to cell cultures as a vehicle control for SB-431542 and GW441756, respectively. (B) Statistical assessment of neurite extension in PC12 cells co-cultured with SCDC2 cells. Data represent the mean ± standard deviation (n=8). * P

    Techniques Used: Immunostaining, Staining, Cell Culture, Co-Culture Assay, Standard Deviation

    Nerve growth factor secreted by SCDC2 cells subsequent to TGF-β1 stimulation promoted the expression of TH mRNA in PC12 cells. SCDC2 cells (7×10 4 cells) and rat pheochromocytoma cells PC12 cells (3.5×10 4 cells) were co-cultured and stimulated with or without TGF-β1 (10 ng/ml) for 24 h. The relative expression level of TH was evaluated using reverse transcription-quantitative polymerase chain reaction in cells also treated with (A) ATPγS (100 µ M), and with (B) TGF-β type I receptor inhibitor SB-431542 (10 µ M), TrkA inhibitor GW441756 (2 nM), IL-1β (10 ng/ml) or TNF-α (10 ng/ml) during the co-culture. Dimethyl sulfoxide was added to cell cultures as a vehicle control for SB-431542 and GW441756, respectively. Data represent the mean ± standard deviation (n=6). * P
    Figure Legend Snippet: Nerve growth factor secreted by SCDC2 cells subsequent to TGF-β1 stimulation promoted the expression of TH mRNA in PC12 cells. SCDC2 cells (7×10 4 cells) and rat pheochromocytoma cells PC12 cells (3.5×10 4 cells) were co-cultured and stimulated with or without TGF-β1 (10 ng/ml) for 24 h. The relative expression level of TH was evaluated using reverse transcription-quantitative polymerase chain reaction in cells also treated with (A) ATPγS (100 µ M), and with (B) TGF-β type I receptor inhibitor SB-431542 (10 µ M), TrkA inhibitor GW441756 (2 nM), IL-1β (10 ng/ml) or TNF-α (10 ng/ml) during the co-culture. Dimethyl sulfoxide was added to cell cultures as a vehicle control for SB-431542 and GW441756, respectively. Data represent the mean ± standard deviation (n=6). * P

    Techniques Used: Expressing, Cell Culture, Real-time Polymerase Chain Reaction, Co-Culture Assay, Standard Deviation

    TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells in Smad2/3-dependent and p38 MAPK-dependent manners. Effects of (A) SIS3 (10 µ M), and (B) SB203580 (10 µ M) on expression of NGF mRNA were evaluated as described in Materials and methods. Data represent the mean ± standard deviation (n=6). * P
    Figure Legend Snippet: TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells in Smad2/3-dependent and p38 MAPK-dependent manners. Effects of (A) SIS3 (10 µ M), and (B) SB203580 (10 µ M) on expression of NGF mRNA were evaluated as described in Materials and methods. Data represent the mean ± standard deviation (n=6). * P

    Techniques Used: Expressing, Standard Deviation

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    Alomone Labs recombinant rat ngf
    <t>TGF-β1</t> promoted the mRNA expression of <t>NGF</t> in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P
    Recombinant Rat Ngf, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/recombinant rat ngf/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    recombinant rat ngf - by Bioz Stars, 2022-09
    93/100 stars
      Buy from Supplier

    94
    Alomone Labs neurotrophin 4 5
    <t>TGF-β1</t> promoted the mRNA expression of <t>NGF</t> in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P
    Neurotrophin 4 5, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/neurotrophin 4 5/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    neurotrophin 4 5 - by Bioz Stars, 2022-09
    94/100 stars
      Buy from Supplier

    Image Search Results


    TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P

    Journal: International Journal of Molecular Medicine

    Article Title: IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals

    doi: 10.3892/ijmm_2018.3714

    Figure Lengend Snippet: TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P

    Article Snippet: Recombinant human TGF-β1 was obtained from PeproTech, Inc. (Rocky Hill, NJ, USA), recombinant rat NGF was obtained from Alomone Labs (Jerusalem, Israel), and recombinant rat IL-1β and TNF-α were purchased from Miltenyi Biotec GmbH (Bergisch Gladbach, Germany).

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Standard Deviation

    IL-1β and TNF-α suppressed the TGF-β1-induced mRNA expression of NGF in SCDC2 cells by abrogating Smad2/3 and p38 MAPK activities. The effects of IL-1β and TNF-α on TGF-β1-induced mRNA expression of NGF in SCDC2 cells were evaluated using RT-qPCR. The cells were treated with or without (A) IL-1β alone or (B) TNF-α alone at indicated concentrations, (C) TGF-β1 (10 ng/ml) and/or IL-1β (10 ng/ml), and (D) TGF-β1 (10 ng/ml) and/or TNF-α (10 ng/ml). Data represent the mean ± standard deviation (n=6). * P

    Journal: International Journal of Molecular Medicine

    Article Title: IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals

    doi: 10.3892/ijmm_2018.3714

    Figure Lengend Snippet: IL-1β and TNF-α suppressed the TGF-β1-induced mRNA expression of NGF in SCDC2 cells by abrogating Smad2/3 and p38 MAPK activities. The effects of IL-1β and TNF-α on TGF-β1-induced mRNA expression of NGF in SCDC2 cells were evaluated using RT-qPCR. The cells were treated with or without (A) IL-1β alone or (B) TNF-α alone at indicated concentrations, (C) TGF-β1 (10 ng/ml) and/or IL-1β (10 ng/ml), and (D) TGF-β1 (10 ng/ml) and/or TNF-α (10 ng/ml). Data represent the mean ± standard deviation (n=6). * P

    Article Snippet: Recombinant human TGF-β1 was obtained from PeproTech, Inc. (Rocky Hill, NJ, USA), recombinant rat NGF was obtained from Alomone Labs (Jerusalem, Israel), and recombinant rat IL-1β and TNF-α were purchased from Miltenyi Biotec GmbH (Bergisch Gladbach, Germany).

    Techniques: Expressing, Quantitative RT-PCR, Standard Deviation

    TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells in Smad2/3-dependent and p38 MAPK-dependent manners. Effects of (A) SIS3 (10 µ M), and (B) SB203580 (10 µ M) on expression of NGF mRNA were evaluated as described in Materials and methods. Data represent the mean ± standard deviation (n=6). * P

    Journal: International Journal of Molecular Medicine

    Article Title: IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals

    doi: 10.3892/ijmm_2018.3714

    Figure Lengend Snippet: TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells in Smad2/3-dependent and p38 MAPK-dependent manners. Effects of (A) SIS3 (10 µ M), and (B) SB203580 (10 µ M) on expression of NGF mRNA were evaluated as described in Materials and methods. Data represent the mean ± standard deviation (n=6). * P

    Article Snippet: Recombinant human TGF-β1 was obtained from PeproTech, Inc. (Rocky Hill, NJ, USA), recombinant rat NGF was obtained from Alomone Labs (Jerusalem, Israel), and recombinant rat IL-1β and TNF-α were purchased from Miltenyi Biotec GmbH (Bergisch Gladbach, Germany).

    Techniques: Expressing, Standard Deviation

    TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P

    Journal: International Journal of Molecular Medicine

    Article Title: IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals

    doi: 10.3892/ijmm_2018.3714

    Figure Lengend Snippet: TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P

    Article Snippet: Reagents Recombinant human TGF-β1 was obtained from PeproTech, Inc. (Rocky Hill, NJ, USA), recombinant rat NGF was obtained from Alomone Labs (Jerusalem, Israel), and recombinant rat IL-1β and TNF-α were purchased from Miltenyi Biotec GmbH (Bergisch Gladbach, Germany).

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Standard Deviation

    IL-1β and TNF-α suppressed the TGF-β1-induced mRNA expression of NGF in SCDC2 cells by abrogating Smad2/3 and p38 MAPK activities. The effects of IL-1β and TNF-α on TGF-β1-induced mRNA expression of NGF in SCDC2 cells were evaluated using RT-qPCR. The cells were treated with or without (A) IL-1β alone or (B) TNF-α alone at indicated concentrations, (C) TGF-β1 (10 ng/ml) and/or IL-1β (10 ng/ml), and (D) TGF-β1 (10 ng/ml) and/or TNF-α (10 ng/ml). Data represent the mean ± standard deviation (n=6). * P

    Journal: International Journal of Molecular Medicine

    Article Title: IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals

    doi: 10.3892/ijmm_2018.3714

    Figure Lengend Snippet: IL-1β and TNF-α suppressed the TGF-β1-induced mRNA expression of NGF in SCDC2 cells by abrogating Smad2/3 and p38 MAPK activities. The effects of IL-1β and TNF-α on TGF-β1-induced mRNA expression of NGF in SCDC2 cells were evaluated using RT-qPCR. The cells were treated with or without (A) IL-1β alone or (B) TNF-α alone at indicated concentrations, (C) TGF-β1 (10 ng/ml) and/or IL-1β (10 ng/ml), and (D) TGF-β1 (10 ng/ml) and/or TNF-α (10 ng/ml). Data represent the mean ± standard deviation (n=6). * P

    Article Snippet: Reagents Recombinant human TGF-β1 was obtained from PeproTech, Inc. (Rocky Hill, NJ, USA), recombinant rat NGF was obtained from Alomone Labs (Jerusalem, Israel), and recombinant rat IL-1β and TNF-α were purchased from Miltenyi Biotec GmbH (Bergisch Gladbach, Germany).

    Techniques: Expressing, Quantitative RT-PCR, Standard Deviation

    Nerve growth factor secreted by SCDC2 cells following TGF-β1 stimulation promoted neurite extension from the surface of ATPγS-treated PC12 cells. (A) Neurite extension of PC12 cells was visualized by immunostaining (×200 magnification; scale bar, 50 µ m) with anti-neurofilament H antibody (red) and nuclei were stained with DAPI (blue). SCDC2 cells (2×10 4 cells) and rat pheochromocytoma cells PC12 (1×10 4 cells) were co-cultured and treated with or without TGF-β1 (10 ng/ml) for 4 days. Cells were also treated with TGF-β type I receptor inhibitor SB-431542 (10 µ M), TrkA inhibitor GW441756 (2 nM), IL-1β (10 ng/ml), or TNF-α (10 ng/ml) from the beginning of the co-culture. In addition, ATPγS (100 µ M) was added to all cultures during cell seeding. Dimethyl sulfoxide was added to cell cultures as a vehicle control for SB-431542 and GW441756, respectively. (B) Statistical assessment of neurite extension in PC12 cells co-cultured with SCDC2 cells. Data represent the mean ± standard deviation (n=8). * P

    Journal: International Journal of Molecular Medicine

    Article Title: IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals

    doi: 10.3892/ijmm_2018.3714

    Figure Lengend Snippet: Nerve growth factor secreted by SCDC2 cells following TGF-β1 stimulation promoted neurite extension from the surface of ATPγS-treated PC12 cells. (A) Neurite extension of PC12 cells was visualized by immunostaining (×200 magnification; scale bar, 50 µ m) with anti-neurofilament H antibody (red) and nuclei were stained with DAPI (blue). SCDC2 cells (2×10 4 cells) and rat pheochromocytoma cells PC12 (1×10 4 cells) were co-cultured and treated with or without TGF-β1 (10 ng/ml) for 4 days. Cells were also treated with TGF-β type I receptor inhibitor SB-431542 (10 µ M), TrkA inhibitor GW441756 (2 nM), IL-1β (10 ng/ml), or TNF-α (10 ng/ml) from the beginning of the co-culture. In addition, ATPγS (100 µ M) was added to all cultures during cell seeding. Dimethyl sulfoxide was added to cell cultures as a vehicle control for SB-431542 and GW441756, respectively. (B) Statistical assessment of neurite extension in PC12 cells co-cultured with SCDC2 cells. Data represent the mean ± standard deviation (n=8). * P

    Article Snippet: Reagents Recombinant human TGF-β1 was obtained from PeproTech, Inc. (Rocky Hill, NJ, USA), recombinant rat NGF was obtained from Alomone Labs (Jerusalem, Israel), and recombinant rat IL-1β and TNF-α were purchased from Miltenyi Biotec GmbH (Bergisch Gladbach, Germany).

    Techniques: Immunostaining, Staining, Cell Culture, Co-Culture Assay, Standard Deviation

    Nerve growth factor secreted by SCDC2 cells subsequent to TGF-β1 stimulation promoted the expression of TH mRNA in PC12 cells. SCDC2 cells (7×10 4 cells) and rat pheochromocytoma cells PC12 cells (3.5×10 4 cells) were co-cultured and stimulated with or without TGF-β1 (10 ng/ml) for 24 h. The relative expression level of TH was evaluated using reverse transcription-quantitative polymerase chain reaction in cells also treated with (A) ATPγS (100 µ M), and with (B) TGF-β type I receptor inhibitor SB-431542 (10 µ M), TrkA inhibitor GW441756 (2 nM), IL-1β (10 ng/ml) or TNF-α (10 ng/ml) during the co-culture. Dimethyl sulfoxide was added to cell cultures as a vehicle control for SB-431542 and GW441756, respectively. Data represent the mean ± standard deviation (n=6). * P

    Journal: International Journal of Molecular Medicine

    Article Title: IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals

    doi: 10.3892/ijmm_2018.3714

    Figure Lengend Snippet: Nerve growth factor secreted by SCDC2 cells subsequent to TGF-β1 stimulation promoted the expression of TH mRNA in PC12 cells. SCDC2 cells (7×10 4 cells) and rat pheochromocytoma cells PC12 cells (3.5×10 4 cells) were co-cultured and stimulated with or without TGF-β1 (10 ng/ml) for 24 h. The relative expression level of TH was evaluated using reverse transcription-quantitative polymerase chain reaction in cells also treated with (A) ATPγS (100 µ M), and with (B) TGF-β type I receptor inhibitor SB-431542 (10 µ M), TrkA inhibitor GW441756 (2 nM), IL-1β (10 ng/ml) or TNF-α (10 ng/ml) during the co-culture. Dimethyl sulfoxide was added to cell cultures as a vehicle control for SB-431542 and GW441756, respectively. Data represent the mean ± standard deviation (n=6). * P

    Article Snippet: Reagents Recombinant human TGF-β1 was obtained from PeproTech, Inc. (Rocky Hill, NJ, USA), recombinant rat NGF was obtained from Alomone Labs (Jerusalem, Israel), and recombinant rat IL-1β and TNF-α were purchased from Miltenyi Biotec GmbH (Bergisch Gladbach, Germany).

    Techniques: Expressing, Cell Culture, Real-time Polymerase Chain Reaction, Co-Culture Assay, Standard Deviation

    TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells in Smad2/3-dependent and p38 MAPK-dependent manners. Effects of (A) SIS3 (10 µ M), and (B) SB203580 (10 µ M) on expression of NGF mRNA were evaluated as described in Materials and methods. Data represent the mean ± standard deviation (n=6). * P

    Journal: International Journal of Molecular Medicine

    Article Title: IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals

    doi: 10.3892/ijmm_2018.3714

    Figure Lengend Snippet: TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells in Smad2/3-dependent and p38 MAPK-dependent manners. Effects of (A) SIS3 (10 µ M), and (B) SB203580 (10 µ M) on expression of NGF mRNA were evaluated as described in Materials and methods. Data represent the mean ± standard deviation (n=6). * P

    Article Snippet: Reagents Recombinant human TGF-β1 was obtained from PeproTech, Inc. (Rocky Hill, NJ, USA), recombinant rat NGF was obtained from Alomone Labs (Jerusalem, Israel), and recombinant rat IL-1β and TNF-α were purchased from Miltenyi Biotec GmbH (Bergisch Gladbach, Germany).

    Techniques: Expressing, Standard Deviation