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. 2019 Nov 7;294(51):19723–19739. doi: 10.1074/jbc.RA119.009744

Figure 7.

Figure 7.

α-SMA–dependent TRPC6 regulates collagen type I expression in Ang II–treated cardiac fibroblasts. Cardiac fibroblasts were transiently transfected with α-SMA siRNA or scrambled siRNA (control). A and B, following exposure of the transfected cells to Ang II for 12 h, collagen α1(I) protein expression was examined by Western blot analysis and normalized to β-actin. ***, p < 0.001 versus control; ###, p < 0.001 versus Ang II. C and D, following exposure of the transfected cells to Ang II for 12 h, TRPC6 protein expression was examined by Western blot analysis and normalized to β-actin. ***, p < 0.001 versus control; ###, p < 0.001 versus Ang II. E and F, cardiac fibroblasts were transiently transfected with TRPC6 siRNA or scrambled siRNA (control). Following exposure of the transfected cells to Ang II for 12 h, collagen type I protein expression was examined by Western blot analysis and normalized to β-actin. ***, p < 0.001 versus control; ###, p < 0.001 versus Ang II. G and H, cardiac fibroblasts were transiently co-transfected with α-SMA siRNA and TRPC6 plasmid overexpression vector. Following revival of the transfected cells and serum deprivation, cardiac fibroblasts were exposed to Ang II for 12 h. Collagen α1(I) protein expression was examined by Western blot analysis and normalized to β-actin. ***, p < 0.001 versus control; ###, p < 0.001 versus Ang II; †††, p < 0.001 versus Ang II + α-SMA siRNA; ns, not significant versus Ang II. Data are representative of three independent experiments (n = 3). Error bars, S.D.