Hypertrophic differentiation is not only the terminal process of endochondral ossification in the growth plate but is also an important pathological change in osteoarthritic cartilage.Collagen type II(COL2A1)was previ...Hypertrophic differentiation is not only the terminal process of endochondral ossification in the growth plate but is also an important pathological change in osteoarthritic cartilage.Collagen type II(COL2A1)was previously considered to be only a structural component of the cartilage matrix,but recently,it has been revealed to be an extracellular signaling molecule that can significantly suppress chondrocyte hypertrophy.However,the mechanisms by which COL2A1 regulates hypertrophic differentiation remain unclear.In our study,a Col2a1 p.Gly1170Ser mutant mouse model was constructed,and Col2a1 loss was demonstrated in homozygotes.Loss of Col2a1 was found to accelerate chondrocyte hypertrophy through the bone morphogenetic protein(BMP)-SMAD1 pathway.Upon interacting with COL2A1,integrinβ1(ITGB1),the major receptor for COL2A1,competed with BMP receptors for binding to SMAD1 and then inhibited SMAD1 activation and nuclear import.COL2A1 could also activate ITGB1-induced ERK1/2 phosphorylation and,through ERK1/2-SMAD1 interaction,it further repressed SMAD1 activation,thus inhibiting BMP-SMAD1-mediated chondrocyte hypertrophy.Moreover,COL2A1 expression was downregulated,while chondrocyte hypertrophic markers and BMP-SMAD1 signaling activity were upregulated in degenerative human articular cartilage.Our study reveals novel mechanisms for the inhibition of chondrocyte hypertrophy by COL2A1 and suggests that the degradation and decrease in COL2A1 might initiate and promote osteoarthritis progression.展开更多
AIM:To investigate the expressions of type I collagen, α2 integrin and β1 integrin in the posterior sclera of guinea pigs with defocus myopia and whether basic fibroblast growth factor (bFGF) injection inhibits the ...AIM:To investigate the expressions of type I collagen, α2 integrin and β1 integrin in the posterior sclera of guinea pigs with defocus myopia and whether basic fibroblast growth factor (bFGF) injection inhibits the formation and development of myopia by upregulating the expression of type I collagen, α2 integrin and β1 integrin. METHODS:After 14 days of treatment, the refractive state and axial length were measured and the levels of type I collagen, α2 integrin and β1 integrin were assayed in the posterior sclerae of groups of guinea pigs that wore a monocular-7D polymethylmethacrylate (PMMA) lens or had -7D lens wear followed by the peribulbar injection of Phosphate Buffer Solution (PBS) or bFGF. The untreated fellow eye served as a control. Guinea pigs with no treatment served as normal group. ·RESULTS:The results showed that 14 days of monocular defocus increased axial eye length and refraction, while bFGF delivery inhibited them markedly. Further, it was also found that the monocular-7D lens could decrease the levels of type I collagen, α2 integrin and β1 integrin expressions, while, unlike PBS, bFGF increased them significantly in comparison to contralateral control eyes and normal eyes. CONCLUSION:bFGF can prevent the formation anddevelopment of defocus myopia by upregulating the expressions of type I collagen, α2 integrin and β1 integrin. Taken together, our results demonstrate that bFGF promotes sclera remodeling to prevent myopia in guinea pigs.展开更多
In this work, the influence of different substrate adhesion during phorbol-12-myristate-13-acetate (PMA)-induced differentiation of THP-1 monocytic cell line was studied. In particular, by morphocytochemical and cytom...In this work, the influence of different substrate adhesion during phorbol-12-myristate-13-acetate (PMA)-induced differentiation of THP-1 monocytic cell line was studied. In particular, by morphocytochemical and cytometric approaches, the influence of type I and type IV collagens in an experimental model representative of three phases (initial, intermediate and terminal) of monocyte-macrophage transition was analyzed. The cells in these three phases of differentiation were obtained by using 6, 30 e 60 nM PMA. In this experimental model, referring to adhesion to glass as control, by using the azo-dye coupling method, we have considered the analysis of Acid Phosphatase (AcP) activity as a marker of differentiated status expression, in relation to the acquisition of macrophagic phenotype. Endosomal/lysosomal system was further characterized by taking into account the uptake of fluorescent probe LysoTracker Red. Fluorochromization in the various experimental conditions was analyzed morphologically (fluorescence microscopy) and quantitatively (static cytometry). Data related to lysosome compartment were integrated, from a cytokinetic point of view, by flow cytometry measurements of DNA/protein content. Our results have indicated that type I and type IV collagens were able to influence, with respect to glass adhesion, various differentiation phases. Type I collagen showed the higher effects in the condition of high differentiation (60 nM PMA), causing an increase in AcP activity and lysosomal system. Type IV collagen, besides determining effects on lysosomal compartment of intermediate and terminally differentiated cells, influenced mainly proliferative activity of cells with initial differentiation level (6 nM PMA).展开更多
Objective To investigate the effects of TGF- β1 on proliferation and type N collagen mRNAexpression of rat renal interstitial libroblasts in vitro for elucidating the role of fibroblasts in renal interstitialfibrosis...Objective To investigate the effects of TGF- β1 on proliferation and type N collagen mRNAexpression of rat renal interstitial libroblasts in vitro for elucidating the role of fibroblasts in renal interstitialfibrosis. Methods The cells were cultured in media containing various concentrations of TGF- β1. Theproliferation and the type Ⅲ collagen mRNA expression of the cells were assayed with MTT method andRT- PCR respectively. Results TGF- β1, has a stimulating proliferation effect with dose- dependence and aincreasing expression of type Ⅲ collagen mRNA with both dose- and time- dependence to the renal fibroblasts. Conclusion It is suggested that TGF- β, is involved in proliferation of renal fibroblasts and their type Ⅲcollagen mRNA expression, and may play an important role in renal interstitial fibrosis.展开更多
目的:探讨微环境中Ⅸ型胶原α1(collagen type IX alpha 1 chain,COL9A1)在结直肠腺癌中的表达及其与肿瘤进展的相关性和临床意义。方法:收集2012年1月至2021年1月手术切除的结直肠癌标本408例,采用免疫组织化学检测结直肠腺癌肿瘤组织...目的:探讨微环境中Ⅸ型胶原α1(collagen type IX alpha 1 chain,COL9A1)在结直肠腺癌中的表达及其与肿瘤进展的相关性和临床意义。方法:收集2012年1月至2021年1月手术切除的结直肠癌标本408例,采用免疫组织化学检测结直肠腺癌肿瘤组织及癌旁正常组织中COL9A1表达,同时检测肿瘤组织中肿瘤蛋白53(tumor protein 53,P53)和错配修复(mismatch repair,MMR)蛋白MLH1、MSH6和PMS2的表达,统计分析COL9A1的表达与各临床病理特征参数的关系,以及与P53突变和MMR状态的相关性,并分析COL9A1阳性表达患者的预后情况。结果:COL9A1在结直肠腺癌肿瘤组织中表达显著低于癌旁正常组织(P<0.001);COL9A1的表达与肿瘤浸润深度、临床分期和肠系膜淋巴结转移有关(χ^(2)=16.943、89.031和84.814;均P<0.001),而与P53突变和MMR状态无关(χ^(2)=0.677、1.260,均P>0.05);Log-rank检验显示COL9A1阴性表达患者的无进展生存期(progression free survival,PFS)和总体生存期(overall survival,OS)显著低于COL9A1阳性表达患者(分别P<0.001,P=0.040)。结论:结直肠腺癌中COL9A1蛋白的表达缺失与肿瘤浸润及转移密切相关,并提示不良预后,这可为结直肠癌预后评估、药物筛选等提供可能的分子标志物和治疗策略。展开更多
The glomerulonephritis disease is characterized by inflammation of glomeruli or small blood vessels in the kidney that causes kidney diseases. The reason of glomerulonephritis disease is to deposit the anti-GBM auto a...The glomerulonephritis disease is characterized by inflammation of glomeruli or small blood vessels in the kidney that causes kidney diseases. The reason of glomerulonephritis disease is to deposit the anti-GBM auto antibody in the glomerular basement membrane. The type IV collagen is the main component of glomerular basement membrane that has α3 chain of type (IV) collagen of non-collagenous domain which contains N-terminal 7S domain, a triple helical collagenous domain and C-terminal non-collagenous glomerular domain (NC1). The amino terminal of α3 (IV) NC1 that induces the Experimental Autoimmuno Glomerulonephritis (EAG) in rat model has been identified. The recombinant rat α3 (IV) NC1 antigen has nine amino acid spans that are consistent with antibody or T cell epitope that induces in EAG. The research is carried out on the recombinant rat α3 (IV) NC1 production, purification, quantification, and characterization. The circulation of anti-GBM antibody in glomerular basement membrane can be measured by the ELISA assay. In addition, the recombinant rat antigen is secreted in HEK293 cell supernatant that is purified by Anti-FLAG M2 monoclonal IgG antibody affinity column and characterized and quantified by SDS-PAGE gel electrophoresis and Western blotting techniques.展开更多
目的:探讨Ⅰ型胶原α1链(collagen type I alpha 1 chain,COL1A1)基因缺失是否抑制卵巢癌细胞的增殖。方法:构建COL1A1基因敲除的载体PX459-COL1A1,转染人卵巢癌ES-2细胞并用嘌呤霉素筛选,获得COL1A1敲除的ES-2细胞。用基因组测序方法检...目的:探讨Ⅰ型胶原α1链(collagen type I alpha 1 chain,COL1A1)基因缺失是否抑制卵巢癌细胞的增殖。方法:构建COL1A1基因敲除的载体PX459-COL1A1,转染人卵巢癌ES-2细胞并用嘌呤霉素筛选,获得COL1A1敲除的ES-2细胞。用基因组测序方法检测COL1A1基因的编辑;细胞增殖、集落形成和细胞迁移实验检测COL1A1缺失对卵巢癌细胞增殖、集落形成及迁移的影响;细胞周期和细胞凋亡实验检测COL1A1缺失对卵巢癌细胞周期和凋亡的影响。裸鼠荷瘤模型体内实验研究COL1A1基因敲除对卵巢癌细胞增殖的影响。结果:Western blot和DNA测序结果显示CRISPR/Cas9方法可以编辑ES-2细胞的COL1A1基因,从而抑制COL1A1蛋白表达。COL1A1缺失显著抑制细胞增殖、软琼脂集落形成能力和细胞迁移(P<0.01)。此外,COL1A1缺失将卵巢癌细胞阻滞于G2期(P<0.01),并促进细胞凋亡(P<0.01)。分子机制研究表明COL1A1缺失可以明显抑制成骨细胞特异性转录因子osterix和基质金属蛋白酶13(matrix metalloproteinase-13, MMP-13)表达(P<0.01),促进聚集蛋白聚糖酶1(aggrecanase-1)表达(P<0.01)。裸鼠荷瘤模型结果表明COL1A1缺失抑制肿瘤生长速度。结论:COL1A1缺失可以通过影响多种基因表达而抑制肿瘤细胞增殖,促进细胞凋亡。展开更多
AIM: To investigate the interfering effect of Y-27632, a ROCK-I selective inhibitor, on the signal transduction pathway of transforming growth factor-beta 1 (TGF-beta 1) in ocular Tenon capsule fibroblasts (OTFS) in v...AIM: To investigate the interfering effect of Y-27632, a ROCK-I selective inhibitor, on the signal transduction pathway of transforming growth factor-beta 1 (TGF-beta 1) in ocular Tenon capsule fibroblasts (OTFS) in vitro. METHODS: After OTFS from passages 4 to 6 47 vitro were induced by TGF-beta 1 and then treated by Y-27632, the changes of the OTFS cell cycles were analyzed via flow cytometry, and the proteins expression of the alpha -smooth muscular actin (alpha -SMA), connective tissue growth factor (CTGF), collagen I were calculated by Western blot. After OTFS treated by the different concentrations of Y-27632, the expression levels of the alpha -SMA, CTGF and collagen I mRNA were assayed by RT-PCR. RESULTS: Y-27632 had no markedly effect on the OTFS cell cycles. After treated by TGF-beta 1, OTFS in G1 period significantly increased. The cell cycles distribution by both TGF-beta 1 and Y-27632 had no remarkable difference from that in control group. Y-27632 significantly inhibited the proteins expressions of both alpha -SMA and CTGF, while to some extent inhibited that of collagen I. TGF-beta 1 significantly promoted the proteins expressions of alpha -SMA, CTGF and collagen I. After OTFS treated by both TGF-beta 1 and Y-27632, of alpha -SMA, the protein expression was similar with that in control group (P=0.066>0.05), but the protein expression of CTGF or collagen I, respectively, was significantly different from that in control group (P=0.000<0.01). The differences of expressions of the alpha -SMA, CTGF and collagen I mRNA in 30, 150, 750 mu mol/L Y-27632 group were statistically significant, compared with those in control group, respectively (alpha -SMA, P=0.002, 0.000, 0.000; CTGF, P=0.014, 0.002, 0.001; collagen I,P=0.003, 0.002, 0.000). CONCLUSION: Blocking the Rho/ROCK signaling pathway by using of Y-27632 could inhibit the cellular proliferation and the expression of both CTGF and alpha -SMA whatever OTFS induced by TGF-beta 1 or not. Y-27632 suppressed the expression of collagen I mRNA without induction.展开更多
基金supported by the National Natural Science Foundation of China (No.81371907,No.81572134,and No.81802217)the China Postdoctoral Science Foundation (No.2017M622873)+2 种基金the Natural Science Foundation of Guangdong Province,China (No.2018A0303130260,No.2016A030313284,and No.2017A030311008)the Guangzhou Science and Technology Plan (No.201804010057)the Fundamental Research Funds for the Central Universities (No.17ykpy06)
文摘Hypertrophic differentiation is not only the terminal process of endochondral ossification in the growth plate but is also an important pathological change in osteoarthritic cartilage.Collagen type II(COL2A1)was previously considered to be only a structural component of the cartilage matrix,but recently,it has been revealed to be an extracellular signaling molecule that can significantly suppress chondrocyte hypertrophy.However,the mechanisms by which COL2A1 regulates hypertrophic differentiation remain unclear.In our study,a Col2a1 p.Gly1170Ser mutant mouse model was constructed,and Col2a1 loss was demonstrated in homozygotes.Loss of Col2a1 was found to accelerate chondrocyte hypertrophy through the bone morphogenetic protein(BMP)-SMAD1 pathway.Upon interacting with COL2A1,integrinβ1(ITGB1),the major receptor for COL2A1,competed with BMP receptors for binding to SMAD1 and then inhibited SMAD1 activation and nuclear import.COL2A1 could also activate ITGB1-induced ERK1/2 phosphorylation and,through ERK1/2-SMAD1 interaction,it further repressed SMAD1 activation,thus inhibiting BMP-SMAD1-mediated chondrocyte hypertrophy.Moreover,COL2A1 expression was downregulated,while chondrocyte hypertrophic markers and BMP-SMAD1 signaling activity were upregulated in degenerative human articular cartilage.Our study reveals novel mechanisms for the inhibition of chondrocyte hypertrophy by COL2A1 and suggests that the degradation and decrease in COL2A1 might initiate and promote osteoarthritis progression.
文摘AIM:To investigate the expressions of type I collagen, α2 integrin and β1 integrin in the posterior sclera of guinea pigs with defocus myopia and whether basic fibroblast growth factor (bFGF) injection inhibits the formation and development of myopia by upregulating the expression of type I collagen, α2 integrin and β1 integrin. METHODS:After 14 days of treatment, the refractive state and axial length were measured and the levels of type I collagen, α2 integrin and β1 integrin were assayed in the posterior sclerae of groups of guinea pigs that wore a monocular-7D polymethylmethacrylate (PMMA) lens or had -7D lens wear followed by the peribulbar injection of Phosphate Buffer Solution (PBS) or bFGF. The untreated fellow eye served as a control. Guinea pigs with no treatment served as normal group. ·RESULTS:The results showed that 14 days of monocular defocus increased axial eye length and refraction, while bFGF delivery inhibited them markedly. Further, it was also found that the monocular-7D lens could decrease the levels of type I collagen, α2 integrin and β1 integrin expressions, while, unlike PBS, bFGF increased them significantly in comparison to contralateral control eyes and normal eyes. CONCLUSION:bFGF can prevent the formation anddevelopment of defocus myopia by upregulating the expressions of type I collagen, α2 integrin and β1 integrin. Taken together, our results demonstrate that bFGF promotes sclera remodeling to prevent myopia in guinea pigs.
文摘In this work, the influence of different substrate adhesion during phorbol-12-myristate-13-acetate (PMA)-induced differentiation of THP-1 monocytic cell line was studied. In particular, by morphocytochemical and cytometric approaches, the influence of type I and type IV collagens in an experimental model representative of three phases (initial, intermediate and terminal) of monocyte-macrophage transition was analyzed. The cells in these three phases of differentiation were obtained by using 6, 30 e 60 nM PMA. In this experimental model, referring to adhesion to glass as control, by using the azo-dye coupling method, we have considered the analysis of Acid Phosphatase (AcP) activity as a marker of differentiated status expression, in relation to the acquisition of macrophagic phenotype. Endosomal/lysosomal system was further characterized by taking into account the uptake of fluorescent probe LysoTracker Red. Fluorochromization in the various experimental conditions was analyzed morphologically (fluorescence microscopy) and quantitatively (static cytometry). Data related to lysosome compartment were integrated, from a cytokinetic point of view, by flow cytometry measurements of DNA/protein content. Our results have indicated that type I and type IV collagens were able to influence, with respect to glass adhesion, various differentiation phases. Type I collagen showed the higher effects in the condition of high differentiation (60 nM PMA), causing an increase in AcP activity and lysosomal system. Type IV collagen, besides determining effects on lysosomal compartment of intermediate and terminally differentiated cells, influenced mainly proliferative activity of cells with initial differentiation level (6 nM PMA).
文摘Objective To investigate the effects of TGF- β1 on proliferation and type N collagen mRNAexpression of rat renal interstitial libroblasts in vitro for elucidating the role of fibroblasts in renal interstitialfibrosis. Methods The cells were cultured in media containing various concentrations of TGF- β1. Theproliferation and the type Ⅲ collagen mRNA expression of the cells were assayed with MTT method andRT- PCR respectively. Results TGF- β1, has a stimulating proliferation effect with dose- dependence and aincreasing expression of type Ⅲ collagen mRNA with both dose- and time- dependence to the renal fibroblasts. Conclusion It is suggested that TGF- β, is involved in proliferation of renal fibroblasts and their type Ⅲcollagen mRNA expression, and may play an important role in renal interstitial fibrosis.
文摘目的:探讨微环境中Ⅸ型胶原α1(collagen type IX alpha 1 chain,COL9A1)在结直肠腺癌中的表达及其与肿瘤进展的相关性和临床意义。方法:收集2012年1月至2021年1月手术切除的结直肠癌标本408例,采用免疫组织化学检测结直肠腺癌肿瘤组织及癌旁正常组织中COL9A1表达,同时检测肿瘤组织中肿瘤蛋白53(tumor protein 53,P53)和错配修复(mismatch repair,MMR)蛋白MLH1、MSH6和PMS2的表达,统计分析COL9A1的表达与各临床病理特征参数的关系,以及与P53突变和MMR状态的相关性,并分析COL9A1阳性表达患者的预后情况。结果:COL9A1在结直肠腺癌肿瘤组织中表达显著低于癌旁正常组织(P<0.001);COL9A1的表达与肿瘤浸润深度、临床分期和肠系膜淋巴结转移有关(χ^(2)=16.943、89.031和84.814;均P<0.001),而与P53突变和MMR状态无关(χ^(2)=0.677、1.260,均P>0.05);Log-rank检验显示COL9A1阴性表达患者的无进展生存期(progression free survival,PFS)和总体生存期(overall survival,OS)显著低于COL9A1阳性表达患者(分别P<0.001,P=0.040)。结论:结直肠腺癌中COL9A1蛋白的表达缺失与肿瘤浸润及转移密切相关,并提示不良预后,这可为结直肠癌预后评估、药物筛选等提供可能的分子标志物和治疗策略。
文摘The glomerulonephritis disease is characterized by inflammation of glomeruli or small blood vessels in the kidney that causes kidney diseases. The reason of glomerulonephritis disease is to deposit the anti-GBM auto antibody in the glomerular basement membrane. The type IV collagen is the main component of glomerular basement membrane that has α3 chain of type (IV) collagen of non-collagenous domain which contains N-terminal 7S domain, a triple helical collagenous domain and C-terminal non-collagenous glomerular domain (NC1). The amino terminal of α3 (IV) NC1 that induces the Experimental Autoimmuno Glomerulonephritis (EAG) in rat model has been identified. The recombinant rat α3 (IV) NC1 antigen has nine amino acid spans that are consistent with antibody or T cell epitope that induces in EAG. The research is carried out on the recombinant rat α3 (IV) NC1 production, purification, quantification, and characterization. The circulation of anti-GBM antibody in glomerular basement membrane can be measured by the ELISA assay. In addition, the recombinant rat antigen is secreted in HEK293 cell supernatant that is purified by Anti-FLAG M2 monoclonal IgG antibody affinity column and characterized and quantified by SDS-PAGE gel electrophoresis and Western blotting techniques.
文摘目的:探讨Ⅰ型胶原α1链(collagen type I alpha 1 chain,COL1A1)基因缺失是否抑制卵巢癌细胞的增殖。方法:构建COL1A1基因敲除的载体PX459-COL1A1,转染人卵巢癌ES-2细胞并用嘌呤霉素筛选,获得COL1A1敲除的ES-2细胞。用基因组测序方法检测COL1A1基因的编辑;细胞增殖、集落形成和细胞迁移实验检测COL1A1缺失对卵巢癌细胞增殖、集落形成及迁移的影响;细胞周期和细胞凋亡实验检测COL1A1缺失对卵巢癌细胞周期和凋亡的影响。裸鼠荷瘤模型体内实验研究COL1A1基因敲除对卵巢癌细胞增殖的影响。结果:Western blot和DNA测序结果显示CRISPR/Cas9方法可以编辑ES-2细胞的COL1A1基因,从而抑制COL1A1蛋白表达。COL1A1缺失显著抑制细胞增殖、软琼脂集落形成能力和细胞迁移(P<0.01)。此外,COL1A1缺失将卵巢癌细胞阻滞于G2期(P<0.01),并促进细胞凋亡(P<0.01)。分子机制研究表明COL1A1缺失可以明显抑制成骨细胞特异性转录因子osterix和基质金属蛋白酶13(matrix metalloproteinase-13, MMP-13)表达(P<0.01),促进聚集蛋白聚糖酶1(aggrecanase-1)表达(P<0.01)。裸鼠荷瘤模型结果表明COL1A1缺失抑制肿瘤生长速度。结论:COL1A1缺失可以通过影响多种基因表达而抑制肿瘤细胞增殖,促进细胞凋亡。
基金Shaanxi Province Science and Technology Gongguan Program, China (No.2011-K14-02-03)
文摘AIM: To investigate the interfering effect of Y-27632, a ROCK-I selective inhibitor, on the signal transduction pathway of transforming growth factor-beta 1 (TGF-beta 1) in ocular Tenon capsule fibroblasts (OTFS) in vitro. METHODS: After OTFS from passages 4 to 6 47 vitro were induced by TGF-beta 1 and then treated by Y-27632, the changes of the OTFS cell cycles were analyzed via flow cytometry, and the proteins expression of the alpha -smooth muscular actin (alpha -SMA), connective tissue growth factor (CTGF), collagen I were calculated by Western blot. After OTFS treated by the different concentrations of Y-27632, the expression levels of the alpha -SMA, CTGF and collagen I mRNA were assayed by RT-PCR. RESULTS: Y-27632 had no markedly effect on the OTFS cell cycles. After treated by TGF-beta 1, OTFS in G1 period significantly increased. The cell cycles distribution by both TGF-beta 1 and Y-27632 had no remarkable difference from that in control group. Y-27632 significantly inhibited the proteins expressions of both alpha -SMA and CTGF, while to some extent inhibited that of collagen I. TGF-beta 1 significantly promoted the proteins expressions of alpha -SMA, CTGF and collagen I. After OTFS treated by both TGF-beta 1 and Y-27632, of alpha -SMA, the protein expression was similar with that in control group (P=0.066>0.05), but the protein expression of CTGF or collagen I, respectively, was significantly different from that in control group (P=0.000<0.01). The differences of expressions of the alpha -SMA, CTGF and collagen I mRNA in 30, 150, 750 mu mol/L Y-27632 group were statistically significant, compared with those in control group, respectively (alpha -SMA, P=0.002, 0.000, 0.000; CTGF, P=0.014, 0.002, 0.001; collagen I,P=0.003, 0.002, 0.000). CONCLUSION: Blocking the Rho/ROCK signaling pathway by using of Y-27632 could inhibit the cellular proliferation and the expression of both CTGF and alpha -SMA whatever OTFS induced by TGF-beta 1 or not. Y-27632 suppressed the expression of collagen I mRNA without induction.
