Chemokine‐like factor 1 (CKLF1) aggravates neointimal hyperplasia through activating the NF‐κB /VCAM‐1 pathway

Abstract

Neointimal hyperplasia (NIH) is a complicated inflammatory process contributing to vascular restenosis. The present study aimed to explore whether chemokine‐like factor 1 (CKLF1) aggravates NIH via the nuclear factor‐kappa B (NF‐κB)/vascular cell adhesion molecule‐1 (VCAM‐1) pathway. We found the expression of CKLF1 and VCAM‐1 significantly increased in human carotid plaques compared to the control. In vivo, CKLF1 overexpression induced a thicker neointimal formation and VCAM‐1 expression was correspondingly upregulated. In vitro, CKLF1 activated NF‐κB and induced VCAM‐1 upregulation in human aortic smooth muscle cells (HASMCs). Functional experiments demonstrated that CKLF1 promoted monocyte adhesion and HASMC migration via VCAM‐1. These results suggest CKLF1 accelerates NIH by promoting monocyte adhesion and HASMC migration via the NF‐κB/VCAM‐1 pathway. Our findings contribute to a better understanding of the mechanisms underlying the causality of CKLF1 on NIH and could prove beneficial in designing therapeutic modalities with a focus on CKLF1.

Keywords

• chemokine‐like factor 1
• neointimal hyperplasia
• NF‐κB
• restenosis
• VCAM‐1