Expression of Ki-67 and estrogen receptor in the uterus of mice with autoimmune premature ovarian failure induced by peptide zona pellucida 3 / 南方医科大学学报
Huihua CAI; Xiafei FU; Xuwen REN; Xiazhu CHEN; Dongmei ZHANG; Yuanli HE.
Journal of Southern Medical University
; (12): 992-997, 2015.
Artículo
en Zh
| WPRIM | ID: wpr-355244
<p><b>OBJECTIVE</b>To investigate the histomorphology and the expressions of the proliferation marker Ki-67 and estrogen receptor in the uterus of mice with autoimmune premature ovarian failure (POF) induced by zona pellucida 3 peptide (pZP3).</p><p><b>METHODS</b>Autoimmune POP models were established in 20 female BALB/c mice (7-8 weeks old) by immunization with pZP3 and another 20 mice served as the control group. The POP models were verified by vaginal cytology, serum sex hormones, ovary histomorphology and ZP3 antibody immunohistochemistry. The histomorphology and expressions of Ki-67, estrogen receptor α and estrogen receptor β in the uterus of the mice were detected.</p><p><b>RESULTS</b>Autoimmune POP models were established successfully in 80% of the mice at 8 weeks after the immunization. Compared with those in the control group, the mice in the model group showed a smaller volume of the uterus, thinner endometrium and a reduced number of glands. The luminal epithelial cells, glandular epithelial cells and stromal cells in the uterus of the model mice all presented with a lower expression of Ki-67 than those in the control group, and Ki-67 translocation from the nuclei to the cytoplasm was found in the model group. The luminal epithelial cells, glandular epithelial cells and stromal cells showed positive ERα immunoreactivity in the model group but not in the control group. No obvious ERβ expression was found in the uterus in either of the groups.</p><p><b>CONCLUSION</b>pZP3 can induce autoimmune POP, cause suppressed proliferation of the endometrial epithelial cells and stromal cells, and reduce the cellular expression of ERα in the uterus of mice.</p>
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