Journal
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
Volume 36, Issue 4, Pages 1371-1381Publisher
KARGER
DOI: 10.1159/000430303
Keywords
MicroRNA-155; Atherosclerosis; Inflammation; SOCS1
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Aims: Accumulating evidence suggests that atherosclerotic progression depends on persistent and chronic inflammation in the arterial walls. MicroRNA-155 is reportedly involved in cardiovascular disease and has been implicated as a pro-inflammation regulator. Although some researchers have focused on microRNA-155 as an atherosclerosis regulator, the mechanisms by which microRNA-155 functions as a putative pro-atherosclerosis microRNA are largely unknown. This study aims to analyze microRNA-155' s effects on atherosclerotic inflammation and to explore its mechanism. Methods: MicroRNA-155' s effects on atherosclerotic inflammation were observed along with the expression and activity levels of SOCS1, STAT3 and NF-kappa B though microRNA-155 inhibition or overexpression. Results: Highly expressions of microRNA-155 in oxLDL-stimulated macrophages and atherosclerosis mice were inversely correlated with SOCS1 expression. Ectopic microRNA-155 overexpression significantly promoted inflammatory cytokine and chemokine production and atherosclerosis progression. We then observed microRNA-155' s functional role in the atherosclerotic pathophysiological process in vivo and in vitro. The observation revealed that by enhancing STAT3 and NF-kappa B signaling and facilitating immune inflammation by targeting SOCS1, microRNA-155 plays a promotable role in atherosclerosis progression. Conclusions: microRNA-155 works as a promoter in the atherosclerotic procession. Its mechanism may include enhancing inflammatory response in atherosclerosis by increasing STAT3 and NF-kappa B signaling via targeting SOCS1. Copyright (C) 2015 S. Karger AG, Basel
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