Figure 6
From: TRPC3-GEF-H1 axis mediates pressure overload-induced cardiac fibrosis
Inhibition of TRPC3 attenuates fibrotic response in human iPSC-derived cardiomyocytes or human cardiac fibroblasts.
(a–c) Effect of Pyr3 (1 μM) on induction of fibrosis-related mRNAs (CTGF and TGF-β1 or -β2) by MS in human iPSC-derived cardiomyocytes (n = 3). Cells were subjected to 20% static-MS for 3 h. GAPDH and 18 S ribosomal RNA were used as internal controls. (d–g) Effects of knockdown (d) or pharmacological inhibition (e) of TRPC3 on CTGF mRNA expression (d,e) and α-SMA protein expression (f,g) induced by TGF-β2 stimulation in human cardiac fibroblasts (n = 3). Error bars, s.e.m. *P < 0.05, **P < 0.01. (h) Schema for the mechanism of TRPC3-mediated cardiac fibrosis induced by pressure overload. TRPC3 mediates MS-induced expression of profibrotic factors (CTGF and TGF-β) in cardiomyocytes and TGF-β-induced fibrotic responses of cardiac fibroblasts, partially through Nox2-dependent GEF-H1 activation.
