Department of Obstetrics and Gynecology, 1st Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Med Sci Monit. 2011 Apr;17(4):BR103-9. doi: 10.12659/msm.881710.
It was unclear whether chronic endometrial ischemia contributed to the pathogenesis of thin endometrium and was associated with decreased endometrial stem/progenitor cell. Thus, we explored the role of chronic endometrial ischemia in the pathogenesis of thin endometrium and its effect on endometrial stem/progenitor cells apoptosis.
MATERIAL/METHODS: In vitro, endometrial side population (ESP) cell apoptosis models were built, and apoptosis was quantified by fluorescence-activated cell sorter (FACS) analysis, pou5f1, and c-kit mRNA was detected by qPCR. In vivo, a rat model of chronic endometrial ischemia was induced by performing bilateral uterine artery ligation. TERT and caspase3 were detected by immunohistochemistry. Pou5f1and c-kit mRNA was examined by qPCR. C-kit, caspase3 and telomerase were detected by Western blot.
In the in vitro endometrial SP (ESP) cells apoptosis model, we found that the apoptotic rate was gradually increased with time, prolonging the expression of TERT, and c-kit mRNA was gradually decreased. In the in vivo endometrial SP (ESP) cells apoptosis model, we found that endometrial thickness, luminal epithelium thickness, gland epithelium thickness and the number of glands in the experiment group were significantly decreased compared with those in the control group (P<0.05). The expression levels of c-kit, pou5f1 and telomerase was significantly lower in the experimental group than those in the control group (P<0.05). The expression level of caspase3 was significantly higher in the experimental group compared with that in the control group (P<0.05).
The present work shows that chronic ischemia and chronic endometrial ischemia-associated stem/progenitor cells apoptosis may be responsible for the pathogenesis of thin endometrium.
慢性子宫内膜缺血是否导致薄型子宫内膜的发病机制尚不清楚，且与子宫内膜干细胞/祖细胞减少有关。因此，我们探讨了慢性子宫内膜缺血在薄型子宫内膜发病机制中的作用及其对子宫内膜干细胞/祖细胞凋亡的影响。
在体外，建立子宫内膜侧群（ESP）细胞凋亡模型，通过流式细胞术（FACS）分析定量检测细胞凋亡，qPCR 检测 pou5f1 和 c-kit mRNA。在体内，通过双侧子宫动脉结扎建立慢性子宫内膜缺血大鼠模型。通过免疫组织化学检测 TERT 和 caspase3。通过 qPCR 检测 pou5f1 和 c-kit mRNA。通过 Western blot 检测 c-kit、caspase3 和端粒酶。
在体外子宫内膜 SP（ESP）细胞凋亡模型中，我们发现随着时间的延长，凋亡率逐渐增加，TERT 和 c-kit mRNA 的表达逐渐降低。在体内子宫内膜 SP（ESP）细胞凋亡模型中，与对照组相比，实验组的子宫内膜厚度、腔上皮厚度、腺体上皮厚度和腺体数量均明显减少（P<0.05）。实验组 c-kit、pou5f1 和端粒酶的表达水平明显低于对照组（P<0.05）。实验组 caspase3 的表达水平明显高于对照组（P<0.05）。
本研究表明，慢性缺血和慢性子宫内膜缺血相关的干细胞/祖细胞凋亡可能是导致薄型子宫内膜发病的原因。
