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. 2017 Aug 3;2(15):e93358. doi: 10.1172/jci.insight.93358

Figure 3. Inhibition of TRPC3-Nox2 coupling suppresses DOX-induced cardiomyocyte atrophy and ROS production.

Figure 3

(A and B) Effects of TRPC3-knockdown on DOX-induced cell shrinkage determined by phalloidin staining (A), and ROS production (B) in NRCMs. NRCMs were treated with DOX (3 μM) for 12 h. Cell areas were analyzed using phalloidin staining (n = 3). Scale bars: 20 μm (A); 40 μm (B). (C) Schema for competitive disruption of the TRPC3-Nox2 protein complex by TRPC3 C-terminal minipeptide (C3-C-GFP or C3-C-HA). (D–F) Effects of C3-C-GFP on DOX-induced cardiomyocyte atrophy (D), C3-C-HA on ROS production (E), and C3-C-GFP on Nox2 upregulation and interaction between TRPC3 and Nox2 (F) in H9c2 rat cardiac myoblasts (n = 3-4). Data are shown as the mean ± SEM. Significance was determined using one-way ANOVA followed by Tukey’s comparison test. *P < 0.05.