Fig. 6
From: KLK11 promotes the activation of mTOR and protein synthesis to facilitate cardiac hypertrophy
KLK11 regulates mTOR signaling to target cardiac hypertrophy. a KLK11 knockdown represses the phosphorylation of Akt-mTOR (n = 3). Mouse cardiomyocytes were transfected with siRNA for 24 h, followed by Ang II (1 μM) treatment for an additional 24 h. Representative western blots and quantitative results are shown. **P < 0.01 by one-way ANOVA with Tukey post-hoc test. b KLK11 overexpression promotes phosphorylation of Akt-mTOR (n = 3). Mouse cardiomyocytes were infected with adenovirus for 24 h, followed by Ang II (1 μM) treatment for an additional 24 h. Representative western blots and quantitative results are shown. **P < 0.01 by one-way ANOVA with Tukey post-hoc test. c KLK11 knockdown represses the phosphorylation of Akt-mTOR in vivo (n = 3). One week–old male C57BL/6 mice received a single intravenous injection of saline or AAV9 vector via the jugular vein. Eight weeks later, the mice received a TAC or sham surgery. Heart tissues from hypertrophic hearts with/without KLK11 knockdown were analyzed. Representative western blots and quantitative results are shown. **P < 0.01 by one-way ANOVA with Tukey post-hoc test. d Rapamycin represses KLK11-mediated phosphorylation of S6K1 and 4EBP1 (n = 3). Mouse cardiomyocytes were infected with adenovirus for 24 h, followed by Ang II (1 μM) treatment in the presence of rapamycin (100 nM) for an additional 24 h. Representative western blots and quantitative results are shown. **P < 0.01 by one-way ANOVA with Tukey post-hoc test. e Rapamycin represses KLK11-mediated protein synthesis (n = 3). Mouse cardiomyocytes were infected with adenovirus for 24 h, followed by protein synthesis by monitoring [3H]-leucine incorporation in the presence of Ang II (1 μM) and rapamycin (100 nM). ***P < 0.001 by one-way ANOVA with Tukey post-hoc test. f Rapamycin represses KLK11-mediated cardiomyocyte hypertrophic growth (n = 3). Mouse cardiomyocytes were infected with adenovirus for 24 h, followed by Ang II (1 μM) treatment in the presence of rapamycin (100 nM) for an additional 48 h. ***P < 0.001 by one-way ANOVA with Tukey post-hoc test. g Rapamycin represses KLK11-mediated overexpression of hypertrophic genes (n = 3). Mouse cardiomyocytes were infected with adenovirus for 24 h, followed by Ang II (1 μM) treatment in the presence of rapamycin (100 nM) for an additional 48 h. ***P < 0.001 by one-way ANOVA with Tukey post-hoc test