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. 2021 Jun 24;9:693079. doi: 10.3389/fcell.2021.693079

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Copyright © 2021 Zhang, Chen, Sun, Zhang, Zhang, Li, Huang, Yang and Ye.

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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A schematic model of SENP3 function in glucocorticoid-induced PPARγ2 signaling. Exogenous glucocorticoid increases the cellular ROS level of BM-MSCs and the protein level of SENP3. SENP3 deSUMOylates SUMO2/3 modification of PPARγ2 on Lys residue 107 site and enhanced its activity to promote the expression of adipogenic marker genes such as C/EBPα, adiponectin and FABP4. Therefore, SENP3 potentiates adipogenesis in BM-MSCs and aggravate glucocorticoid-induced osteoporosis under oxidative stress.