雌二醇通过ERα抑制miR-16表达并促进蜕膜间充质干细胞生长

发布时间：2019-01-07 08:25

【摘要】：目的:研究雌二醇(E2)通过调控微小RNA-16(miR-16)的表达对胎盘蜕膜来源间充质干细胞(MSCs)活力的影响。方法:分别检测E2在正常孕妇及重度子痫前期(PE)患者外周血中的浓度。CCK-8法分析不同浓度E2对MSCs活力的影响。Real-time PCR分析不同浓度E2处理MSCs对miR-16表达的影响。探索E2通过何种受体调控miR-16表达。结果:与正常孕妇相比,重度PE患者外周血中E2浓度显著降低(P0.01)。5、10和100 nmol/L E2分别处理MSCs 48 h后,MSCs活力显著增加(P0.05)。5、10和100 nmol/L E2分别处理MSCs12 h后,miR-16的表达水平下调(P0.05),而用10 nmol/L E2处理MSCs不同时间(0 h、3 h、6 h、12 h和24 h)后,miR-16表达水平随着时间呈现明显下调趋势。在E2处理之前预先转染miR-16,细胞活力被显著逆转。E2处理MSCs之前6 h,用雌激素受体拮抗剂ICI 182780和他莫昔芬预预处理,E2对miR-16失去抑制作用。雌激素受体α(ERα)激动剂丙基吡唑三醇(PPT)及ERβ受体激动剂二芳基丙腈DPN分别处理MSCs后,仅PPT可明显抑制miR-16表达。结论:雌二醇可能通过ERα抑制miR-16表达,从而促进蜕膜MSCs的生长。
[Abstract]:Aim: to study the effect of estradiol (E2) on the (MSCs) activity of placental decidual derived mesenchymal stem cells by regulating the expression of tiny RNA-16 (miR-16). Methods: the concentrations of E2 in peripheral blood of normal pregnant women and patients with severe preeclampsia (PE) were detected respectively. The effect of E2 at different concentrations on MSCs activity was analyzed by CCK-8 method. The effect of MSCs treated with different concentrations of E2 on miR-16 expression was analyzed by Real-time PCR. To explore the receptors through which E2 regulates the expression of miR-16. Results: compared with normal pregnant women, the concentration of E _ 2 in peripheral blood of patients with severe PE was significantly lower than that of normal pregnant women (P0.01). After treated with MSCs for 48 h, the activity of MSCs increased significantly (P0.05). The expression level of miR-16 was down-regulated (P0.05), but the expression of miR-16 was down-regulated with time after MSCs was treated with 10 nmol/L E2 (0 h, 3 h, 6 h, 12 h and 24 h). The activity of miR-16, cells pretransfected before E2 treatment was significantly reversed. After pretreatment with estrogen receptor antagonist ICI 182780 and tamoxifen at 6 h before E2 treatment, E2 had no inhibitory effect on miR-16. After MSCs was treated with estrogen receptor 伪 (ER 伪) agonist propylpyrazoltriol (PPT) and ER 尾 receptor agonist diarylpropionitrile (DPN), only PPT could significantly inhibit miR-16 expression. Conclusion: estradiol may inhibit the expression of miR-16 through ER 伪 and promote the growth of decidua MSCs.
【作者单位】：南京大学医学院附属鼓楼医院;
【基金】：国家自然科学基金资助项目(No.81401223)
【分类号】：R714.244

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