Fig. 3
From: KLK11 promotes the activation of mTOR and protein synthesis to facilitate cardiac hypertrophy
KLK11 regulates cardiac hypertrophy in vitro. a siRNA knockdown of KLK11 in cardiomyocytes (n = 3). Mouse cardiomyocytes were transfected with siCtrl or siKLK11 for 48 h. mRNA and protein levels of KLK11 were analyzed. ***P < 0.001 by unpaired Student’s t test. b KLK11 knockdown reduces Ang II-induced hypertrophic growth of cardiomyocytes (n = 3). Mouse cardiomyocytes were transfected with siCtrl or siKLK11 for 24 h, followed by Ang II (1 μM) treatment for an additional 48 h. Representative images for a-actinin staining and quantitative results are shown. **P < 0.01 by one-way ANOVA with Tukey post-hoc test. c KLK11 knockdown reduces Ang II-induced overexpression of hypertrophic genes in cardiomyocytes (n = 3). Mouse cardiomyocytes were transfected with siCtrl or siKLK11 for 24 h, followed by Ang II (1 μM) treatment for an additional 48 h. **P < 0.01 by one-way ANOVA with Tukey post-hoc test. d Adenovirus-mediated overexpression of KLK11 in cardiomyocytes (n = 3). Mouse cardiomyocytes were infected with AdCtrl or AdKLK11 for 48 h. mRNA and protein levels of KLK11 were analyzed. ***P < 0.001 by unpaired Student’s t test. e KLK11 overexpression promoted Ang II-induced hypertrophic growth of cardiomyocytes (n = 3). Mouse cardiomyocytes were infected with AdCtrl or AdKLK11 for 24 h, followed by Ang II (1 μM) treatment for an additional 48 h. Representative images for a-actinin staining and quantitative results are shown. **P < 0.01 by one-way ANOVA with Tukey post-hoc test. f KLK11 overexpression promoted Ang II-induced overexpression of hypertrophic genes in cardiomyocytes (n = 3). Mouse cardiomyocytes were infected with AdCtrl or AdKLK11 for 24 h, followed by Ang II (1 μM) treatment for an additional 48 h. **P < 0.01 by one-way ANOVA with Tukey post-hoc test