OBJECTIVE: This study aims to investigate the role and mechanism of miR-365 in the coronary atherosclerosis (AS). PATIENTS AND METHODS: Blood were collected from AS patients and healthy people, coronary plaque and adjacent arterial tissue were collected from AS patients. QRT-PCR method was used to detect expressions of miR-365 and IL-6 in coronary plaque, blood monocytes, and serum. Western blot was applied to detect IL-6 protein expression in coronary plaque and blood monocytes, and ELISA was used to detect IL-6 protein expression in serum. RESULTS: Compared with the normal group, IL-6 expression was significantly increased in coronary plaque, blood monocytes, and serum both in mRNA level and in protein level, while miR-365 expression was significantly decreased (p < 0.05). CONCLUSIONS: IL-6 expression was significantly up-regulated in coronary plaque, blood monocytes, and serum, whereas miR-365 expression was down-regulated. MiR-365 may regulate the pathogenesis and immune response in AS through targeting IL-6.
OBJECTIVE: This study aims to investigate the role and mechanism of miR-365 in the coronary atherosclerosis (AS). PATIENTS AND METHODS: Blood were collected from AS patients and healthy people, coronary plaque and adjacent arterial tissue were collected from AS patients. QRT-PCR method was used to detect expressions of miR-365 and IL-6 in coronary plaque, blood monocytes, and serum. Western blot was applied to detect IL-6 protein expression in coronary plaque and blood monocytes, and ELISA was used to detect IL-6 protein expression in serum. RESULTS: Compared with the normal group, IL-6 expression was significantly increased in coronary plaque, blood monocytes, and serum both in mRNA level and in protein level, while miR-365 expression was significantly decreased (p < 0.05). CONCLUSIONS:IL-6 expression was significantly up-regulated in coronary plaque, blood monocytes, and serum, whereas miR-365 expression was down-regulated. MiR-365 may regulate the pathogenesis and immune response in AS through targeting IL-6.