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. 2020 Nov 26;13(1):493–515. doi: 10.18632/aging.202159

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Copyright: © 2020 Yang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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MICU1 mediated cardiomyocyte hypertrophy by modulating oxidation states. (A, B) The ROS levels in cardiomyocytes treated with Ang-II and MICU1 siRNA were analyzed by DHE staining. Representative confocal microscope images (A) and fluorescence quantitation (B) were presented. Scale bars=10 μm. (C) ROS generation in cardiomyocytes treated with Ang-II and MICU1 siRNA was detected by an ELISA kit. (D, E) The ROS levels in NMVMs treated with Ang-II and Ad-MICU1 were analyzed by DHE staining. Representative confocal microscope images (D) and fluorescence quantitation (E) were presented. Scale bars=10 μm. (F) ROS generation in cardiomyocytes treated with Ang-II and Ad-MICU1 was detected by an ELISA kit. Presented values are means ± SEM. N=6-8/group. ^**P<0.01 vs. Normal (1); ^##P<0.01 vs. M scRNA of Ang-II; ^&&P<0.01 vs. Normal (2); ^ΨΨP<0.01 vs. Ad-EV of Ang-II.