Research Paper Volume 13, Issue 10 pp 13788—13806

Redd1 knockdown prevents doxorubicin-induced cardiac senescence

Dox exposure upregulates Redd1 expression in both cardiac tissue and cultured cardiomyocytes. (A, B) Representative photomicrographs and quantitative analysis of cardiac p16INK4a immunofluorescent staining in control and Dox-treated mice (n = 6 per group). (C, D) Representative photomicrographs and quantitative analysis of cardiac p21 immunofluorescent staining in control and Dox-treated mice (n = 6 per group). (E, F) Western blotting detection and quantification of Redd1, p16INK4a, and p21 expression in cardiac tissue from control and Dox-treated mice (n = 6–8 per group). (G, H) Time-course expression and quantification analysis of Redd1, p16INK4a, and p21 protein levels in cultured H9c2 cardiomyocytes treated with Dox (0.1 μM) (n = 3 samples per group). Data are mean ± SEM. *p

Figure 2. Dox exposure upregulates Redd1 expression in both cardiac tissue and cultured cardiomyocytes. (A, B) Representative photomicrographs and quantitative analysis of cardiac p16INK4a immunofluorescent staining in control and Dox-treated mice (n = 6 per group). (C, D) Representative photomicrographs and quantitative analysis of cardiac p21 immunofluorescent staining in control and Dox-treated mice (n = 6 per group). (E, F) Western blotting detection and quantification of Redd1, p16INK4a, and p21 expression in cardiac tissue from control and Dox-treated mice (n = 6–8 per group). (G, H) Time-course expression and quantification analysis of Redd1, p16INK4a, and p21 protein levels in cultured H9c2 cardiomyocytes treated with Dox (0.1 μM) (n = 3 samples per group). Data are mean ± SEM. *p < 0.05 vs. control group.