Figure 5
From: TRPC3-GEF-H1 axis mediates pressure overload-induced cardiac fibrosis
Involvement of microtubule stability in TRPC3/Nox2-mediated GEF-H1 activation.
(a) Representative images of microtubule organization in rat cardiac fibroblasts with or without TGF-β2 (2 ng/mL) for 6 h, in the presence or absence of Pyr3 (1 μM). Right panels were magnified views indicated with white boxes. Bar graph represents the semi-quantitative results of microtubule densities (n = 6). (b,c) Effects of knockdown (b) or pharmacological inhibition (c) of Nox2 on GEF-H1 activation induced by MS. NRCMs were subjected to 20% static-MS for 10 min (n = 3). (d) Involvement of tubulin stability on MS-induced GEF-H1 activation in NRCMs. NRCMs were treated with taxol (1 μM) 30 min prior to 20% static-MS for 10 min (n = 3). (e) Effect of Nox2 knockdown on MS-induced GEF-H1 activation in NRCMs. NRCMs were treated with okadaic acid (0.1 μM) 30 min prior to 20% static-MS for 10 min (n = 3). Error bars, s.e.m. *P < 0.05, **P < 0.01.
