MicroRNA-126, -145, and -155
Author(s) -
Yuanyuan Wei,
Maliheh Nazari-Jahantigh,
Peter Neth,
Christian Weber,
Andreas Schober
Publication year - 2013
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.112.300279
Subject(s) - microrna , biology , medicine , genetics , gene
Atherosclerosis is a condition caused by lipid-induced inflammation of the vessel wall orchestrated by a complex interplay of various cell types, such as endothelial cells, smooth muscle cells, and macrophages. MicroRNAs (miRNAs) have emerged as key regulators of gene expression typically by repressing the target mRNA, which determines cell fate and function under homeostatic and disease conditions. Here, we outline the effects of miRNA-145, -126, and -155 in atherosclerosis in vivo. Downregulation of miR-145, which controls differentiation of smooth muscle cells, promotes lesion formation, whereas the endothelial cell-specific miRNA-126 signals the need for endothelial repair through its transfer from apoptotic endothelial cells in microvesicles. Elevated miR-155 levels are characteristic of proinflammatory macrophages and atherosclerotic lesions. However, the effects of miR-155 seem to be different in early and advanced atherosclerosis. The discovery of the role of these miRNAs in atherosclerosis sheds light on the current concepts of atherogenesis and may provide novel treatment options for cardiovascular diseases.
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