MicroRNA-155 in the pathogenesis of atherosclerosis: a conflicting role?

Atherosclerosis is widely appreciated to involve a chronic lipid-induced inflammatory reaction of the arterial wall in response to haemodynamic stress and dyslipidaemia. The dysfunction of resident vascular cells and recruitment of infiltrating leukocyte cells orchestrate a complex interplay in the initiation and development of atherosclerosis. Despite a great many advances in recent years, the detailed mechanisms modulating the inflammation in atherosclerosis have not been fully elucidated. MicroRNAs (miRNAs) are small non-coding RNA (ncRNA) molecules that regulate gene expression post-transcriptionally by degradation and translational repression of target messenger RNAs (mRNAs). Substantial evidence demonstrates that miRNAs play a vital role in the physiological control of gene expression and in the pathogenesis of malignant, infectious, and cardiovascular disorders. MiR-155, a typical multi-functional miRNA, has recently emerged as a novel component of inflammatory signal transduction in the pathogenesis of atherosclerosis. MiR-155-mediated regulation is extensively involved in endothelial cells (ECs), macrophages, dendritic cell (DCs), vascular smooth muscle cells (VSMCs) and differentiation of leukocyte subsets. MiR-155 can modulate the expression of genes correlated with inflammation in different cell types in vitro and also affect the atherogenesis in vivo. However, miR-155 appears to play a conflicting role in the disease pathogenesis. Besides, miR-155 is potentially applied as a novel disease biomarker and therapeutic target in diagnosing and treating atherosclerosis. This article reviews the pertinent literature and mechanisms of action of miR-155 that have thus far been associated with atherosclerosis. Here we first introduce in brief the basic knowledge of the miRNA regulation and later discuss with emphasis the regulatory role of miR-155 in various cell types involved in atherosclerosis.