Carbon Monoxide Releasing Molecule Accelerates Reendothelialization after Carotid Artery Balloon Injury in Rat.
- Author:
Qing Song HU
1
;
Yang Xin CHEN
1
;
Qing Sheng HUANG
1
;
Bing Qing DENG
1
;
Shuang Lun XIE
1
;
Jing Feng WANG
1
;
Ru Qiong NIE
1
Author Information
- Publication Type:Journal Article
- Keywords: Carbon monoxide; Neointima formation; Reendothelialization; Vascular injury
- MeSH: Animals; Carbon Monoxide; metabolism; pharmacology; Carotid Artery Injuries; drug therapy; immunology; metabolism; pathology; Carotid Artery, Common; drug effects; immunology; metabolism; pathology; Cell Adhesion; drug effects; Disease Models, Animal; Endothelial Cells; drug effects; immunology; metabolism; pathology; Endothelium, Vascular; drug effects; metabolism; pathology; Humans; Male; Rats; Rats, Sprague-Dawley
- From: Biomedical and Environmental Sciences 2015;28(4):253-262
- CountryChina
- Language:English
-
Abstract:
OBJECTIVEThis study was aimed to investigate the effects of carbon monoxide releasing molecule (CORM-2), a novel carbon monoxide carrier, on the reendothelialization of carotid artery in rat endothelial denudation model.
METHODSMale rats subjected to carotid artery balloon injury were treated with CORM-2, inactive CORM-2 (iCORM-2) or dimethyl sulfoxide (DMSO). The reendothelialization capacity was evaluated by Evans Blue dye and the immunostaining with anti-CD31 antibody. The number of circulating endothelial progenitor cells (EPCs) was detected by flow cytometry. The proliferation, migration, and adhesion of human umbilical vein endothelial cells (HUVECs) were assessed by using [3H]thymidine, Boyden chamber and human fibronectin respectively. The expressions of protein were detected by using western blot analysis.
RESULTSCORM-2 remarkably accelerated the re-endothelialization 5 d later and inhibited neointima formation 28 d later. In addition, the number of peripheral EPCs significantly increased in CORM-2-treated rats than that in iCORM-2 or DMSO-treated rats after 5 d later. In vitro experiments, CORM-2 significantly enhanced the proliferation, migration and adhesion of HUVECs. The levels of Akt, eNOS phosphorylation, and NO generation in HUVECs were also much higher in CORM-2 treated group. Blocking of PI3K/Akt/eNOS signaling pathway markedly suppressed the enhanced migration and adhesion of HUVECs induced by CORM-2.
CONCLUSIONCORM-2 could promote endothelial repair, and inhibit neointima formation after carotid artery balloon injury, which might be associated with the function changes of HUVECs regulated by PI3K/Akt/eNOS pathway.
