Chemokine‐like factor 1 (CKLF1) aggravates neointimal hyperplasia through activating the NF‐κB /VCAM‐1 pathway
Xinnong Liu,
Chengjia Qu,
Yongbao Zhang,
Jie Fang,
Lequn Teng,
Rujiao Zhang,
Xiangyu Zhang,
Chenyang Shen
Affiliations
Xinnong Liu
Vascular Surgery Center State Key Laboratory of Cardiovascular Disease National Center for Cardiovascular Diseases Fuwai Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China
Chengjia Qu
Vascular Surgery Center State Key Laboratory of Cardiovascular Disease National Center for Cardiovascular Diseases Fuwai Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China
Yongbao Zhang
Vascular Surgery Center State Key Laboratory of Cardiovascular Disease National Center for Cardiovascular Diseases Fuwai Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China
Jie Fang
Vascular Surgery Center State Key Laboratory of Cardiovascular Disease National Center for Cardiovascular Diseases Fuwai Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China
Lequn Teng
Vascular Surgery Center State Key Laboratory of Cardiovascular Disease National Center for Cardiovascular Diseases Fuwai Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China
Rujiao Zhang
College of Clinical Medicine Hebei University Baoding China
Xiangyu Zhang
Department of General Surgery Sir Run Run Shaw Hospital Zhejiang University School of Medicine Hangzhou China
Chenyang Shen
Vascular Surgery Center State Key Laboratory of Cardiovascular Disease National Center for Cardiovascular Diseases Fuwai Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Beijing China
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.
