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T. Fujimoto, M. Inoue-Mochida, T. Inoue, N. Ohtsu, T. Kameda, N. Kasaoka, K. Kimoto, H. Tanihara; RhoA/ROCK Pathway Mediated the Expression of Type1 Collagen Induced by TGF-β2 in Trabecular Meshwork Cells. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3211. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
Transforming growth factor (TGF)-β2 is reported to cause the increase of intraocular pressure in glaucoma by inducing the accumulation of extracellular matrix (ECM) in the trabecular meshwork (TM). The aim of this study is to examine whether the RhoA/ROCK pathway is involved in TGF-β2-induced collagen expression in a human TM cells (HTM) and porcine TM cells (PTM).
The effect of TGF-β2 on RhoA activation was evaluated by pull-down assay. Transcriptional activities of the COL1A2 were evaluated by dual-luciferase reporter assay with the induction of constitutive active RhoA. The effect of selective ROCK inhibitor, Y27632, on type I collagen synthesis induced by TGF-β2 was assessed by ELISA.
RhoA was activated at 30 min after stimulation with 2.5 ng/ml TGF-β2 in PTM and HTM. Relative RhoA activities were 2.9 and 3.5-fold increased in PTM and HTM respectively. Transcriptional activities of COL1A2 were 1.3-fold increased by TGF-β2 stimulation. Similarly, constitutive active RhoA increased COL1A2 promoter activity. Type 1 collagen in the HTM culture medium was 1.8-fold increased at 48 hours after stimulation with TGF-β2. Combined treatment withTGF-β2 and Y-27632 showed 1.2-fold increase in culture medium when compared with untreated HTM..
These results suggest that the RhoA/ROCK pathway plays a role in relaying TGF-β2 signal transduction to type I collagen synthesis in TM.
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