Estradiol promotes growth of decidua derived mesenchymal stem cells by inhibiting miR-16 via estrogen receptorα
10.3969/j.issn.1000-4718.2017.12.018
- VernacularTitle: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
- Author:
Ying ZHANG
1
;
feng Guang ZHAO
;
Jie LI
Author Information
1. 南京大学医学院附属鼓楼医院,江苏南京210008
- Keywords:
Estradiol;
MicroRNA-16;
Preeclampsia;
Mesenchymal stem cells
- From:
Chinese Journal of Pathophysiology
2017;33(12):2227-2232
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To study the effect of estradiol (E2) on the viability of mesenchymal stem cells (MSCs) de-rived from the decidua of the placenta by regulating the expression of microRNA-16 (miR-16).METHODS:The concen-tration of E2 in the peripheral blood of normal pregnant women and the patients with severe preeclampsia ( PE) was meas-ured.The effects of E2 at different concentrations on the viability of MSCs were analyzed .The effect of E2 at different con-centrations on the expression of miR-16 in the MSCs was detected , and which estrogen receptor ( ER) mediated the regula-tory effect of E2 on miR-16 expression was determined .RESULTS:The concentration of E2 in peripheral blood of the pa-tients with severe PE was significantly decreased (P<0.01).After treatment with E2 at 5, 10 and 100 nmol/L for 48 h, the viability of MSCs was increased (P<0.05).The expression level of miR-16 was down-regulated in the MSCs treated with E2 at 5, 10 and 100 nmol/L for 12 h.After treatment with E2 at 10 nmol/L for different time (0 h, 3 h, 6 h, 12 h and 24 h) , the expression level of miR-16 in the MSCs showed a clear time-dependent downward trend .E2 significantly promoted the viability of MSCs , and the cell viability was significantly reversed after miR-16 pretreatment.Pretreatment with estrogen receptor antagonists ICI 182780 and tamoxifen for 6 h attenuated the inhibitory effect of E 2 on miR-16 expres-sion.Only ERαagonist propyl pyrazole triol significantly inhibited the expression of miR-16 in MSCs but ERβagonist dia-rylpropionitrile did not .CONCLUSION:E2 promotes the growth of decidua-derived MSCs by inhibiting miR-16 via ERα.
