[No authors listed]
Atherosclerosis is the primary cause of cardiovascular and cerebrovascular diseases. Recent studies have revealed that CâXâC motif chemokine ligand 16 (CXCL16), microRNA (miR)â146a and miRâ146b may have important roles in atherosclerotic diseases. However, the associations of CXCL16, miRâ146a and miRâ146b in atherosclerotic diseases in vivo remain unclear. Previous studies have demonstrated that miRâ146a and miRâ146b may negatively regulate the toll like receptor (TLR4)/nuclear factor (NF)âκB signaling pathway to repress the inflammatory response. The present study investigated the associations of CXCL16, miRâ146a and miRâ146b in atherosclerotic apolipoprotein E (ApoE)â/â mice in vivo. The expression levels of CXCL16, TLR4/NFâκB signaling pathway, miRâ146a and miRâ146b in the control and atherosclerotic ApoEâ/â mice were investigated via reverse transcriptionâquantitative polymerase chain reaction and western blot analysis. The present study demonstrated that the expression of CXCL16 was significantly upregulated in atherosclerotic ApoEâ/â mice compared with control ApoEâ/â mice. The expression levels of TRL4, interleukinâ1 receptorâassociated kinase 1, tumor necrosis factor receptor associated factor 6, NFâκB, tumor necrosis factorâα and interleukinâ1β were also significantly upregulated in atherosclerotic ApoEâ/â mice compared with control mice. However, the present study revealed that the expression levels of miRâ146a and miRâ146b were significantly downregulated in atherosclerotic ApoEâ/â mice compared with control ApoEâ/â mice. Overall, the results of the present study suggested that CXCL16 may regulate the TRL4/NFâκB/CXCL16 signaling pathway, and that miRâ146a and miRâ146b may negatively regulate CXCL16 via this pathway in atherosclerosis in vivo.
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