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miR‐16 inhibits the proliferation and angiogenesis‐regulating potential of mesenchymal stem cells in severe pre‐eclampsia
Author(s) -
Wang Yaping,
Fan Hongye,
Zhao Guangfeng,
Liu Dan,
Du Leilei,
Wang Zhiqun,
Hu Yali,
Hou Yayi
Publication year - 2012
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.12037
Subject(s) - mesenchymal stem cell , angiogenesis , microbiology and biotechnology , stem cell , biology , decidua , amniotic stem cells , endothelial stem cell , trophoblast , cancer research , adult stem cell , immunology , placenta , fetus , genetics , pregnancy , in vitro
Pre‐eclampsia is thought to be a systemic disease of maternal endothelial cell dysfunctions. mi RNA s regulate various basic biological functions in cells, including stem cells. Mesenchymal stem cells exist in almost all tissues and are the key cellular source for tissue repair and regeneration. Our aims are to investigate whether mi RNA s regulate MSC s in fetal–maternal interfaces to influence the pathogenesis of pre‐eclampsia. The differential expression of mi RNA s in decidua‐derived mesenchymal stem cells of all patients with severe pre‐eclampsia ( n = 20) and normal groups ( n = 20) was first screened by microarray analysis and validated by quantitative real‐time PCR analysis. The integrated bioinformatics analysis showed that miR‐16 showed the highest number of connections in the mi RNA GO network and the mi RNA gene network. Moreover, over‐expressed miR‐16 inhibited the proliferation and migration of decidua‐derived mesenchymal stem cells and induced cell‐cycle arrest by targeting cyclin E1. Interestingly, over‐expression of miR‐16 by decidua‐derived mesenchymal stem cells reduced the ability of human umbilical vein endothelial cells to form blood vessels and reduced the migration of trophoblast cells. Furthermore, decidua‐derived mesenchymal stem cell‐expressed endothelial growth factor VEGF‐A was involved in migration of trophoblast cells and human umbilical vein endothelial cells as well as tube and network formation. Importantly, the levels of cyclin E1 and VEGF‐A were negatively correlated with the level of miR‐16 expression in decidua‐derived mesenchymal stem cells from the patients with severe pre‐eclampsia. Together, these data suggest that the alteration of miR‐16 expression in decidua‐derived mesenchymal stem cells may be involved in the development of pre‐eclampsia.