Figure 4
From: TRPC3-GEF-H1 axis mediates pressure overload-induced cardiac fibrosis
Inhibition of TRPC3 attenuates TGF-β-induced myofibroblast transdifferentiation of neonatal rat cardiac fibroblasts.
(a) Representative α-SMA-stained images of rat cardiac fibroblasts. Cells were treated with Pyr3 (1 μM) for 20 min prior to treatment with TGF-β2 (2 ng/mL) for 48 h (n = 3). (b,c) Effect of Pyr3 (1 μM) on TGF-β2 (2 ng/mL for 6 h)-induced CTGF mRNA expression (b) and [3H] proline incorporation (c) in fibroblasts (n = 3). (d) Effects of TRPC3 knockdown on [3H] proline incorporation in fibroblasts with or without Ang II (100 nM), endothelin-1 (ET-1; 100 nM) or TGF-β2 (n = 3). (e,f) Effects of TRPC3 knockdown on GEF-H1 (e) and RhoA (f) activation induced by TGF-β2 for 6 h. (n = 3) (g) Effects of GEF-H1 knockdown on the TGF-β2-induced increase in α-SMA expression (n = 3). Error bars, s.e.m. *P < 0.05, **P < 0.01.
