Publications (2)8.4 Total impact
-
Article: MiR-16 inhibits the proliferation and angiogenesis-regulating potential of mesenchymal stem cells in severe pre-eclampsia.
[show abstract] [hide abstract]
ABSTRACT: Pre-eclampsia (PE) is thought to be a systemic disease of maternal endothelial cell dysfunctions. MicroRNA (miRNAs) can regulate various basic biological functions in cells including stem cells. Mesenchymal stem cells (MSCs) exist in almost all tissues and are the key cellular source for tissue repair and regeneration. Our aims are to investigate whether miRNAs regulate MSCs in fetal-maternal interfaces to influence the pathogenesis of PE. The differential expressions of miRNAs in decidua-derived MSCs (dMSCs) of sPE (n=20) and normal groups (n=20) were firstly screened by microarray analysis and validated by quantitative real-time PCR (qRT-PCR) analysis. The integrated bioinformatics analysis showed that miR-16 was the highest degree in miRNA-GO-network and miRNA-Gene-network. Moreover, over-expressed miR-16 inhibited the proliferation and migration of dMSCs and induced the cell cycle arrest by targeting cyclinE1 (CCNE1). Interestingly, MiR-16-over-expressed dMSCs reduced the ability of human umbilical vein endothelial cell (HUVEC) to form blood vessels and the migration of the trophoblast cells (HTR-8). Furthermore, dMSCs-expressed VEGF-A was involved in the migration of HTR-8 cells and HUVEC as well as tube and network formation. Importantly, the levels of CCNE1 and VEGFA were negatively correlated with the level of miR-16 expression in dMSCs from the same patient of severe PE. Together, these data suggest that the alteration of miR-16 expression in dMSCs may be involved in the development of PE. This work may provide a new molecular event in fetal-maternal interfaces to explain the pathogenesis of PE. © 2012 The Authors Journal compilation © 2012 FEBS.FEBS Journal 10/2012; · 3.79 Impact Factor -
Article: microRNA-29b contributes to pre-eclampsia through its effects on apoptosis, invasion and angiogenesis of trophoblast cells.
[show abstract] [hide abstract]
ABSTRACT: PE (pre-eclampsia), a pregnancy-specific disorder, is characterized by increased trophoblast cell death and deficient trophoblast invasion and reduced trophoblast-mediated remodelling of spiral arteries. The present study was performed to determine the function of miR-29b (microRNA-29b) in trophoblast cells and its underlying role in the pathogenesis of PE. The prediction of miR-29b target genes was performed using computer-based programs, including Targetscan, Pictar and miRBase. The function of these target genes was analysed further by gene ontology (GO). The effects of miR-29b on apoptosis, and invasion and angiogenesis of trophoblast cell lines (HTR-8/SVneo, BeWo and JAR) were examined by flow cytometry and Matrigel assay respectively. We found that miR-29b induced apoptosis and inhibited invasion and angiogenesis of trophoblast cells. Further studies confirmed that miR-29b regulated the expression of MCL1 (myeloid cell leukaemia sequence 1), MMP2 (encoding matrix metallproteinase 2), VEGFA (vascular endothelial growth factor A) and ITGB1 (integrin β1) genes by directly binding to their 3'-UTRs (untranslated regions). Moreover, we identified that there was an inverse correlation between miR-29b and its target genes in subjects with PE. Taken together, these findings support a novel role for miR-29b in invasion, apoptosis and angiogenesis of trophoblast cells, and miR-29b may become a new potential therapeutic target for PE.Clinical Science 06/2012; 124(1):27-40. · 4.61 Impact Factor
