Associations of CXCL16, miR‑146a and miR‑146b in atherosclerotic apolipoprotein E‑knockout mice.

Atherosclerosis is the primary cause of cardiovascular and cerebrovascular diseases. Recent studies have revealed that C‑X‑C motif chemokine ligand 16 (CXCL16), microRNA (miR)‑146a and miR‑146b may have important roles in atherosclerotic diseases. However, the associations of CXCL16, miR‑146a and miR‑146b in atherosclerotic diseases in vivo remain unclear. Previous studies have demonstrated that miR‑146a and miR‑146b may negatively regulate the toll like receptor (TLR4)/nuclear factor (NF)‑κB signaling pathway to repress the inflammatory response. The present study investigated the associations of CXCL16, miR‑146a and miR‑146b in atherosclerotic apolipoprotein E (ApoE)‑/‑ mice in vivo. The expression levels of CXCL16, TLR4/NF‑κB signaling pathway, miR‑146a and miR‑146b in the control and atherosclerotic ApoE‑/‑ mice were investigated via reverse transcription‑quantitative polymerase chain reaction and western blot analysis. The present study demonstrated that the expression of CXCL16 was significantly upregulated in atherosclerotic ApoE‑/‑ mice compared with control ApoE‑/‑ mice. The expression levels of TRL4, interleukin‑1 receptor‑associated kinase 1, tumor necrosis factor receptor associated factor 6, NF‑κB, tumor necrosis factor‑α and interleukin‑1β were also significantly upregulated in atherosclerotic ApoE‑/‑ mice compared with control mice. However, the present study revealed that the expression levels of miR‑146a and miR‑146b were significantly downregulated in atherosclerotic ApoE‑/‑ mice compared with control ApoE‑/‑ mice. Overall, the results of the present study suggested that CXCL16 may regulate the TRL4/NF‑κB/CXCL16 signaling pathway, and that miR‑146a and miR‑146b may negatively regulate CXCL16 via this pathway in atherosclerosis in vivo.