Endothelial dysfunction induced by high glucose is associated with decreased ATP-binding cassette transporter G1 expression.
- Author:
Jiahong XUE
1
;
Xiaolin NIU
;
Jin WEI
;
Xin DONG
;
Canzhan ZHU
;
Yinhu DANG
;
Anqi SONG
;
Huimei HUANG
Author Information
- Publication Type:Journal Article
- MeSH: ATP Binding Cassette Transporter, Sub-Family G, Member 1; ATP-Binding Cassette Transporters; genetics; metabolism; Aorta; cytology; Cell Line; Down-Regulation; drug effects; Endothelial Cells; cytology; metabolism; physiology; Glucose; pharmacology; Humans
- From: Journal of Southern Medical University 2012;32(1):14-18
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of ATP-binding cassette transporter G1 (ABCG1) in endothelial dysfunction induced by high glucose.
METHODSHuman aortic endothelial cells (HAECs) were incubated in the presence of 5.6 or 30 mmol/L glucose for 24-72 h with or without a 2-h pretreatment with the LXR agonist 22(R)-hydroxycholesterol. Real-time PCR and Western blotting were used to measure the mRNA and protein expressions of ABCG1; the intracellular cholesterol efflux and endothelial nitric oxide synthase (eNOS) activity were measured by scintillation counting.
RESULTSHigh glucose time-dependently suppressed ABCG1 expression and cholesterol efflux to HDL in HAECs. High glucose also decreased eNOS activity. ABCG1 down-regulation induced by high glucose, along with decreased cholesterol efflux and eNOS activity, was abolished by treatment of the cells with the LXR agonist.
CONCLUSIONEndothelial dysfunction induced by high glucose is associated with decreased ABCG1 expression.
