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. 2020 Sep 29;8:548605. doi: 10.3389/fcell.2020.548605

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Copyright © 2020 Wang, Lan, Guo, Cai, Wang, Wang, Li, Li, Wang, Li, Wu, Lu and Liu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Downregulation of SESN2 contributed to cardiotoxicity induced by JMJD3 overexpression. SESN2 was overexpressed by adenovirus Ad-SESN2 or knocked out by targeting sgRNA in NRCMs with or without DOX (0.5 μM, 48 h) and JMJN3 co-treatment. (A,E,H) The nuclear condensation in NRCMs was observed by Hoechst staining, scale bar = 100 or 50 μm. (B,F,I) Mitochondrial structure changes of cardiomyocytes was indicated by Mitotracker Red staining, scale bar = 25 μm. (C,D,G) The protein expression of SESN2, cleaved caspase3 and BAX/Bcl2 were analyzed by Western blot. Data were presented as the mean ± SD. (C,D) *p < 0.05, ***p < 0.001 vs. Ad-Flag or CRISPR-V2 group. ^###p < 0.001 vs. Ad-Flag + DOX group. n = 3. (G) *p < 0.05 vs. Ad-GFP group. ^#p < 0.05 vs. Ad-GFP + DOX group. ^&p < 0.05 vs. Ad-JMJD3 + DOX group. n = 3. DOX, doxorubicin; JMJD3, Jumonji domain-containing 3; SESN2, Sestrin2.