Pu, S.; Wang, Q.; Liu, Q.; Zhao, H.; Zhou, Z.; Wu, Q. Effect of Nr1d1 on Serpina3 Mediated Cell Senescence by Nuclear Receptor Nr4a3 in Mouse Heart-Derived Sca-1+CD31− Cells. Preprints2022, 2022010304. https://doi.org/10.20944/preprints202201.0304.v1
APA Style
Pu, S., Wang, Q., Liu, Q., Zhao, H., Zhou, Z., & Wu, Q. (2022). Effect of Nr1d1 on Serpina3 Mediated Cell Senescence by Nuclear Receptor Nr4a3 in Mouse Heart-Derived Sca-1+CD31− Cells. Preprints. https://doi.org/10.20944/preprints202201.0304.v1
Chicago/Turabian Style
Pu, S., Zuping Zhou and Qiong Wu. 2022 "Effect of Nr1d1 on Serpina3 Mediated Cell Senescence by Nuclear Receptor Nr4a3 in Mouse Heart-Derived Sca-1+CD31− Cells" Preprints. https://doi.org/10.20944/preprints202201.0304.v1
Abstract
Aim: Sca-1+CD31− cells were shown to be endothelial stem/progenitor cells, found in many mammalian tissues, including heart, were able to differentiate into cardiomyocytes in vitro and in vivo. Our previous work indicated that heart derived Sca-1+CD31− cells increased Nr1d1 mRNA level and decreased cells plasticity with aging. However, little is known about how NR1D1 affects Sca-1+CD31− cells plasticity. Methods: Lentiviral vector was used to stably overexpress Nr1d1 in young Sca-1+CD31− cells and to knockdown Nr1d1 in aged Sca-1+CD31− cells. Cell differentiation, proliferation, apoptosis, and cell cycle were evaluated. Results and Conclusions: The overexpression of Nr1d1 in young Sca-1+CD31− cells inhibited cell proliferation and promoted apoptosis. Knockdown of Nr1d1 in aged Sca-1+CD31− cells promoted cell proliferation and inhib-ited apoptosis. Using mouse cardiac myocytes cell line, confirmed the effect of Nr1d1 and indi-cated that Nr1d1 induce Serpina3 expression via Nr1d1 interaction with Nr4a3. Nr1d1 may there-fore be identified as a potent anti-aging receptor and be a therapeutic target for aging relative diseases.
Biology and Life Sciences, Cell and Developmental Biology
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