Du Xiao-Hang, Shi Gang, Lü Dong-Hao, Wang Yu-He, Chen Jie-Ting, Zheng Qian, Yin Xia
Department of Obstetrics and Gynecology, West China Second University Hospital, Chengdu 610041, China.
Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University) , Ministry of Education, Chengdu 610041, China.
Sichuan Da Xue Xue Bao Yi Xue Ban. 2018 Jul;49(4):546-550.
To determine the expression of microRNA-221 (miR-221) in endometrial tissues and its impact on the proliferation of ectopic endometrial stromal cells.
Endometrial stromal cells were isolated, cultured and identified from normal endometrial tissues (taken from patients without endometriosis) and ectopic endometrial tissues (taken from patients with ovarian endometriosis). The expression of microRNA-221 was detected by stem-loop qRT-PCR. Changes in the expression of miR-221-3p in endometrial stromal cells exposed to estraldiol (108 mol/L) for 48 h were detected. The effects of miR-221-3p inhibitor on the expressions of miR-221-3p, phosphatase and tensin homology deleted on chromosome ten () and cell proliferations were compared with those of the negative control (NC, 10 nmol/L).
The expression of miR-221-3p in ectopic endometrial tissues was 4.2 times higher than that in normal endometrial tissues (=0.039): 2.66 times higher in ectopic endometrial stromal cells compared with normal endometrial stromal cells (=0.029). But no differences in the expression of miR-221-5p were found (>0.05). No differences in the change of miR-221-3p expression after exposure to estrogen for 48h were found between normal and ectopic stromal cells. Inhibition of miR-221-3p function was associated with decreased cell proliferation (=0.018) and increased expression of gene (=0.021).
The expression of microRNA-221 is upregulated in ectopic endometrial tissues and ectopic endometrial stroma cells. Inhibiting the function of miR-221-3p may result in increased expression and decreased cell proliferation in endometrial stromal cells.
检测微小RNA-221(miR-221)在子宫内膜组织中的表达及其对异位子宫内膜间质细胞增殖的影响。
从正常子宫内膜组织(取自无子宫内膜异位症患者)和异位子宫内膜组织(取自卵巢子宫内膜异位症患者)中分离、培养并鉴定子宫内膜间质细胞。采用茎环定量逆转录聚合酶链反应(stem-loop qRT-PCR)检测miR-221的表达。检测暴露于雌二醇(108 mol/L)48小时的子宫内膜间质细胞中miR-221-3p表达的变化。将miR-221-3p抑制剂对miR-221-3p、第10号染色体上缺失的磷酸酶和张力蛋白同源物(PTEN)表达及细胞增殖的影响与阴性对照(NC,10 nmol/L)进行比较。
异位子宫内膜组织中miR-221-3p的表达比正常子宫内膜组织高4.2倍(P = 0.039);异位子宫内膜间质细胞中miR-221-3p的表达比正常子宫内膜间质细胞高2.66倍(P = 0.029)。但miR-221-5p的表达差异无统计学意义(P>0.05)。正常和异位间质细胞暴露于雌激素48小时后,miR-221-3p表达的变化差异无统计学意义。抑制miR-221-3p功能与细胞增殖减少(P = 0.018)及PTEN基因表达增加(P = 0.021)有关。
miR-221在异位子宫内膜组织和异位子宫内膜间质细胞中表达上调。抑制miR-221-3p功能可能导致子宫内膜间质细胞中PTEN表达增加及细胞增殖减少。