miR-200及其甲基化调节在人早产子宫平滑肌收缩机制中的作用研究

Study on the role of miR-200 and its methylation in contractile mechanism of human premature uterine smooth muscle

目的探讨miR-200及其甲基化调节在早产子宫平滑肌收缩机制中的作用。方法收集2014年1月-2015年12月该院收治的6例早产临产剖宫产孕妇子宫平滑肌作为病例组,6例未临产早产孕妇子宫平滑肌作为对照组。BSP方法检测两组miR-200启动子区域甲基化水平; Real-PCR比较两组miR-200家族表达差异,应用Dot-blot方法检测两组整体子宫平滑肌甲基化差异。结果 miR-200家族在早产临产与未临产子宫平滑肌表达均呈高甲基化状态,但临产未临产miR-200家族表达无明显差异。早产临产子宫平滑肌较早产未临产子宫平滑肌整体基因组呈低甲基化状态;结论早产子宫平滑肌基因组整体呈低甲基化状态,miR-200家族可能不参与早产子宫平滑肌收缩机制的调节。

Objective To explore the role of miR-200 and its methylation in contractile mechanism of human premature uterine smooth muscle. Methods From January 2014 to December 2015,the specimens of uterine smooth muscle of 6 cases of premature labor treated in Obstetrics and Gynecology Hospital of Fudan Unviersity were collected as case group,and the specimens of uterine smooth muscle of 6 cases of normal labor were selected as control group. BSP method was used to detect the methylation levels of miR-200 promoter region. Realtime PCR was used to compare the difference of miR-200 family expression. Dot-blot method was used to detect the difference of overall uterine smooth muscle methylation between the two groups. Results The methylation level of miR-200 family in uterine smooth muscle of cases of premature labor and normal labor were high,but there was no statistically significant difference in the expression of miR-200 family.Compared with cases of normal labor,methylation level of miR-200 family in uterine smooth muscle of cases of premature labor was lower.Conclusion The whole genome of premature uterine smooth muscle shows a low methylation state,miR-200 family may not be involved in the regulation of uterine smooth muscle contraction mechanism in premature labor.