MicroRNA-199a-3p upregulated in atherosclerosis lesions inhibited the inflammation of monocyte

Abstract

Objective To investagate the mechanism of inhibiting chemotaxis and inflammation factors release of monocyte induced by microRNA (miRNA, miR)-199a-3p, which is upregulated and derived by macrophage in Atherosclerosis plaque via exosomes. Methods The expression and distribution of miR-199a-3p in atherosclerosis plaque was detected and analysed via inmmunofluorescence and in situ hybridization. Exosomes were isolated from serum of human peripheral blood and were detected by transmission electron microscopy. The expression of chemokine receptors and inflammation factors in miR-199a-3p mimics-treated-monocyte was detected by reverse transcriptase-polymerase chain reaction (RT-PCR). Results MiR-199a-3p was upregulated in macrophage of atherosclerosis lesions and was derived into peripheral blood via exosomes [control group: (2.343 0±0.282 1)%, treat group: (6.968 0±0.590 1)%, P<0.01]. The exosome-derived miR-199a-3p could inhibite the chemotaxis of monocyte by downregulating the expression of chemokine receptors, very lateantigen-4 (VLA-4) and lymphocyte function-associated antigen-1 (LFA-1). Meanwhile, the exosome-derived miR-199a-3p inhibited the monocyte releasing of inflammation factors, for example, tumor necrosis factor-α (TNF-α) and interleukin (IL)-6. Conclusion MiR-199a-3p upregulated by macrophage of atherosclerosis lesions could inhibit the chemotaxis and inflammation factors release of monocyte in human blood via exosomes. Key words: Atherosclerosis; Exosome; MicroRNA; Monocyte-macrophage