Atherosclerosis (AS) is a chronic inflammation in response to lipid accumulation. Increasing evidence has demonstrated that numerous microRNAs (miRs) have critical roles in inflammatory responses. A previous study suggested that miR‑146b‑5p is possibly associated with AS; however, its exact role has remained largely elusive. The present study aimed to investigate the potential role of miR‑146b‑5p in AS and to explore the underlying mechanism. Fist, the levels of miR‑146b‑5p were determined in foam cells and clinical specimens from patients with AS by reverse‑transcription quantitative PCR. The role of miR‑146b‑5p in AS was then investigated by using miR‑146b‑5p inhibitor. The results demon... More
Atherosclerosis (AS) is a chronic inflammation in response to lipid accumulation. Increasing evidence has demonstrated that numerous microRNAs (miRs) have critical roles in inflammatory responses. A previous study suggested that miR‑146b‑5p is possibly associated with AS; however, its exact role has remained largely elusive. The present study aimed to investigate the potential role of miR‑146b‑5p in AS and to explore the underlying mechanism. Fist, the levels of miR‑146b‑5p were determined in foam cells and clinical specimens from patients with AS by reverse‑transcription quantitative PCR. The role of miR‑146b‑5p in AS was then investigated by using miR‑146b‑5p inhibitor. The results demonstrated that the expression levels of miR‑146b‑5p were elevated in the lesions of patients with AS. In addition, the levels of miR‑146b‑5p in THP‑1 cells stimulated with phorbol 12‑myristate 13‑acetate (100 nM) to induce their differentiation into macrophages were dose‑ and time‑dependently elevated by oxidized low‑density lipoprotein treatment applied for inducing foam cell formation. miR‑146b‑5p was also revealed to directly target tumor necrosis factor receptor‑associated factor 6 (TRAF6), which functions as a signal transducer in the nuclear factor‑κB (NF‑κB) pathway. Furthermore, the present study reported for the first time that miR‑146b‑5p inhibition promotes the inflammatory response and enhances lipid uptake during foam cell formation. In conclusion, miR‑146b‑5p inhibition promoted chronic inflammation and had a detrimental role during AS‑associated foam cell formation by targeting TRAF6.
