Expression of Ki-67 and estrogen receptor in the uterus of mice with autoimmune premature ovarian failure induced by peptide zona pellucida 3
10.3969/j.issn.1673-4254.2015.07.11
- VernacularTitle:透明带3多肽诱导的免疫性卵巢早衰小鼠模型子宫组织中Ki-67、ER的表达
- Author:
Huihua CAI
1
;
Xiafei FU
;
Xuwen REN
;
Xiazhu CHEN
;
Dongmei ZHANG
;
Yuanli HE
Author Information
1. 南方医科大学珠江医院妇产科
- Keywords:
autoimmune premature ovarian failure;
peptide zona pellucida 3;
endometrium;
Ki-67;
estrogen receptor
- From:
Journal of Southern Medical University
2015;(7):992-997
- CountryChina
- Language:Chinese
-
Abstract:
Objective 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). Methods 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 receptorαand estrogen receptorβin the uterus of the mice were detected. Results Autoimmune POP models were estblished 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 ERαimmunoreactivity in the model group but not in the control group. No obvious ERβexpression was found in the uterus in either of the groups. Conclusion pZP3 can induce autoimmune POP, cause suppressed proliferation of the endometrial epithelial cells and stromal cells, and reduce the cellular expression of ERαin the uterus of mice.
