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10.3892/etm.2017.5121

http://scihub22266oqcxt.onion/10.3892/etm.2017.5121
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C5704332!5704332!29201219
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suck abstract from ncbi


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pmid29201219      Exp+Ther+Med 2017 ; 14 (5): 5087-92
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  • Blockade of 146b-5p promotes inflammation in atherosclerosis-associated foam cell formation by targeting TRAF6 #MMPMID29201219
  • Lin N; An Y
  • Exp Ther Med 2017[Nov]; 14 (5): 5087-92 PMID29201219show ga
  • 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-?B (NF-?B) 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.
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