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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Exp+Ther+Med
2017 ; 14
(5
): 5087-5092
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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
): 5087-5092
PMID29201219
show 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.