Journal
MOLECULAR THERAPY
Volume 25, Issue 6, Pages 1279-1294Publisher
CELL PRESS
DOI: 10.1016/j.ymthe.2017.03.031
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Funding
- National Basic Research Program of China [2012CB518601]
- National Natural Science Foundation of China [31271396, 31271224]
- Hebei Natural Science Foundation of China [H2016206406]
- Fok Ying Tung Education Foundation [131037]
- Hebei science and technology project [13967607D]
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The vascular response to pro-atherosclerotic factors is a multi factorial process involving endothelial cells (ECs), macrophages (MACs), and smooth muscle cells (SMCs), although the mechanism by which these cell types communicate with each other in response to environmental cues is yet to be understood. Here, we show that miR-155, which is significantly expressed and secreted in Kriippel-like factor 5 (KLF5)-overexpressing vascular smooth muscle cells (VSMCs), is a potent regulator of endothelium barrier function through regulating endothelial targeting tight junction protein expression. VSMCs-derived exosomes mediate the transfer of KLF5-induced miR-155 from SMCs to ECs, which, in turn, destroys tight junctions and the integrity of endothelial barriers, leading to an increased endothelial permeability and enhanced atherosclerotic progression. Moreover, overexpression of miR-155 in ECs inhibits endothelial cell proliferation/migration and re-endothelialization in vitro and in vivo and thus increases vascular endothelial permeability. Blockage of the exosome-mediated transfer of miR-155 between these two cells may serve as a therapeutic target for atherosclerosis.
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