Journal
CELL CYCLE
Volume 15, Issue 21, Pages 2895-2905Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15384101.2016.1208873
Keywords
apoptosis; EGR1; follicular atresia; granulosa cell; NF-B; ovarian aging
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Funding
- National Natural Science Foundation of China [81370469, 81300453, 81501227]
- Program of International Science and Technology Corporation of China [2013DFA31400]
- Health and Family Planning Commission Research Programs of Hubei Province of China [2015CFB711]
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Follicular atresia is the main process responsible for the loss of follicles and oocytes from the ovary, and it is the root cause of ovarian aging. Apoptosis of granulosa cells (GCs) is the cellular mechanism responsible for follicular atresia in mammals. Recent advances have highlighted fundamental roles for EGR1 in age-related diseases via the induction of apoptosis. In the present study, we found that the expression of EGR1 was significantly increased in aged mouse ovaries compared with young ovaries. Immunohistochemical analysis revealed strongly positive EGR1 staining in atretic follicles, especially in apoptotic granulosa cells. We further showed that EGR1 up-regulation in mouse primary granulosa cells inhibited cell proliferation and promoted apoptosis. In addition, the promotion of apoptosis in GCs by EGR1 increases over time and with reactive oxygen species (ROS) stimulation. Our mechanistic study suggested that EGR1 regulates GC apoptosis in a mitochondria-dependent manner and that this mainly occurs through the NF-B signaling pathway. In conclusion, our results suggested that age-related up-regulation of EGR1 promotes GC apoptosis in follicle atresia during ovarian aging.
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