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. 2015 Dec 1;8(12):1579–1589. doi: 10.1242/dmm.019968

Fig. 2.

Fig. 2.

Nox4 mediates myofibroblast transformation and collagen synthesis via increased oxidative stress. (A) Representative immunoblots showing knockdown of Nox4 expression in control (left panel) and heart failure (HF) cardiac fibroblasts (CFs) (right panel) with Nox4 siRNA (siNox4) vs scrambled control (Scr). GAPDH was used as a loading control. (B) Confocal images of CFs stained with MitoSOX (red) showing inhibition of mitochondrial oxidative stress with siNox4 in control and HF CFs. Nuclei are stained blue with Hoechst 33342. Fluorescence quantitation is shown below those images. *P<0.003 vs Control Scr+No Drug, **P<0.005 vs Scr+No Drug, #P<0.02 vs Scr+TGF-β; n=3-4 in all groups. Scale bar: 20 μm. (C) Representative immunoblots (upper panels) showing the effects of Nox4 knockdown on basal and TGF-β-stimulated α-SMA and collagen I expression in control (left panel) and HF (right panel) CFs. GAPDH was used as a loading control. Densitometric analysis is shown below. *P<0.05 vs Scr+No Drug, **P<0.01 vs Scr+TGF-β, #P=0.05 vs Scr+No Drug; n=3-4 in all groups. (D) Basal and TGF-β-stimulated collagen synthesis in control and HF CFs following transfection with siNox4 or Scr control. *P<0.05 vs Control Scr+No Drug, **P<0.005 vs Scr+TGF-β; #P<0.01 vs HF Scr+No Drug; n=3-4 in all groups.