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

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 ex...

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Main Authors: Xinnong Liu, Chengjia Qu, Yongbao Zhang, Jie Fang, Lequn Teng, Rujiao Zhang, Xiangyu Zhang, Chenyang Shen
Format: Article
Language:English
Published: Wiley 2020-09-01
Series:FEBS Open Bio
Subjects:
Online Access:https://doi.org/10.1002/2211-5463.12942
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author Xinnong Liu
Chengjia Qu
Yongbao Zhang
Jie Fang
Lequn Teng
Rujiao Zhang
Xiangyu Zhang
Chenyang Shen
author_facet Xinnong Liu
Chengjia Qu
Yongbao Zhang
Jie Fang
Lequn Teng
Rujiao Zhang
Xiangyu Zhang
Chenyang Shen
author_sort Xinnong Liu
collection DOAJ
description 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.
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spelling doaj.art-62cb74866087410da384edacaf3b8eb52023-05-23T06:46:11ZengWileyFEBS Open Bio2211-54632020-09-011091880189010.1002/2211-5463.12942Chemokine‐like factor 1 (CKLF1) aggravates neointimal hyperplasia through activating the NF‐κB /VCAM‐1 pathwayXinnong Liu0Chengjia Qu1Yongbao Zhang2Jie Fang3Lequn Teng4Rujiao Zhang5Xiangyu Zhang6Chenyang Shen7Vascular 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 ChinaVascular 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 ChinaVascular 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 ChinaVascular 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 ChinaVascular 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 ChinaCollege of Clinical Medicine Hebei University Baoding ChinaDepartment of General Surgery Sir Run Run Shaw Hospital Zhejiang University School of Medicine Hangzhou ChinaVascular 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 ChinaNeointimal 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.https://doi.org/10.1002/2211-5463.12942chemokine‐like factor 1neointimal hyperplasiaNF‐κBrestenosisVCAM‐1
spellingShingle Xinnong Liu
Chengjia Qu
Yongbao Zhang
Jie Fang
Lequn Teng
Rujiao Zhang
Xiangyu Zhang
Chenyang Shen
Chemokine‐like factor 1 (CKLF1) aggravates neointimal hyperplasia through activating the NF‐κB /VCAM‐1 pathway
FEBS Open Bio
chemokine‐like factor 1
neointimal hyperplasia
NF‐κB
restenosis
VCAM‐1
title Chemokine‐like factor 1 (CKLF1) aggravates neointimal hyperplasia through activating the NF‐κB /VCAM‐1 pathway
title_full Chemokine‐like factor 1 (CKLF1) aggravates neointimal hyperplasia through activating the NF‐κB /VCAM‐1 pathway
title_fullStr Chemokine‐like factor 1 (CKLF1) aggravates neointimal hyperplasia through activating the NF‐κB /VCAM‐1 pathway
title_full_unstemmed Chemokine‐like factor 1 (CKLF1) aggravates neointimal hyperplasia through activating the NF‐κB /VCAM‐1 pathway
title_short Chemokine‐like factor 1 (CKLF1) aggravates neointimal hyperplasia through activating the NF‐κB /VCAM‐1 pathway
title_sort chemokine like factor 1 cklf1 aggravates neointimal hyperplasia through activating the nf κb vcam 1 pathway
topic chemokine‐like factor 1
neointimal hyperplasia
NF‐κB
restenosis
VCAM‐1
url https://doi.org/10.1002/2211-5463.12942
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