摘要
目的:研究不明原因复发性流产(URSA)患者绒毛组织中miR-155表达及其与凋亡分子、血管新生分子的关系。方法:选择URSA患者40例为URSA组,接受人工流产的正常早孕者30例为对照组,收集绒毛组织,检测miR-155以及凋亡分子(Bcl-2、Bcl-xl、Bax、Bad、Fas、FasL)、血管新生分子(HIF-1α、VEGF、sFlt-1)的表达量。结果:URSA组患者绒毛组织中miR-155的表达量显著低于对照组且流产次数越多、miR-155的表达量越低;URSA组患者绒毛组织中促凋亡分子Bax、Bad、Fas、FasL的表达量均高于对照组且与miR-155的表达量呈负相关;抗凋亡基因Bcl-2、Bcl-xl的表达量均低于对照组且与miR-155的表达量呈正相关;URSA组患者绒毛组织中HIF-1α、VEGF的表达量低于对照组且与miR-155的表达量呈正相关,sFlt-1的表达量高于对照组且与miR-155的表达量呈负相关。结论:USRA患者绒毛组织中miR-155呈低表达,miR-155可能通过调节凋亡分子、血管新生分子的表达参与该病的发生、发展。
Objective: To study miR-155 expression in villus tissue of patients with recurrent spontaneous abortion and its relationship with apoptosis molecules and angiogenesis molecules. Methods: A total of 40 cases with unexplained recurrent spontaneous abortion were selected as URSA group, 30 cases of normal early pregnant women receiving artificial abortion were selected as control group, and villus tissue was collected to detect expression levels of miR-155, apoptosis molecules (Bcl 2, Bcl-xl, Bax, Bad, Fas and FasL) and angiogenesis molecules (HIF-1α, VEGF and sFlt-1). Results: miR-155 expression level in villus tissue of URSA group was significantly lower than that of control group. The miR-155 expression level decreased with increase of abortion; pro-apoptosis molecules Bax, Bad, Fas and FasL expression levels in villus tissue of URSA group were higher than those of control group and negatively correlated with miR-155 expression level, and anti-apoptosis genes Bel 2 and Bcl-xl expression levels were lower than those of control group and positively correlated with miR t55 expression level; HIF-1α and VEGF expression levels in villus tissue of URSA group were lower than those of control group and positively correlated with miR-155 expression level, and sFh-1 expression level was higher than that of control group and negatively correlated withmiR-155 expression level. Conclusion.. miR-155 is lowly expressed in villus tissue of patients with recurrent spontaneous abor- tion, and miR-155 may be involved in the occurrence and development of the disease through regulating the expression of apop- tosis molecules and angiogenesis molecules.
出处
《海南医学院学报》
CAS
2016年第5期428-430,434,共4页
Journal of Hainan Medical University
基金
三峡大学培优基金(A2011-302-38)~~