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Effect of Glycated LDL on Monocyte Adhesion on Vascular Endothelial Cells: Role of Plasminogen Activator Inhibitor‐1
Author(s) -
Shen Garry,
Zhao Ruozhi,
Ren Song,
Moghadasian Mohammed
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb484
Subject(s) - monocyte , inflammation , plasminogen activator inhibitor 1 , endothelium , umbilical vein , plasminogen activator , cell adhesion , endocrinology , medicine , chemistry , adhesion , in vitro , biochemistry , organic chemistry
Diabetes accelerates the development of atherosclerotic cardiovascular diseases. Inflammation on endothelium plays a key role in atherosclerosis. Monocyte adhesion is the earliest event of vascular inflammation. Elevated levels of glycated low density lipoprotein (gLDL) were detected in diabetic patients. We previously demonstrated that gLDL increased the expression of plasminogen activator inhibitor‐1 (PAI‐1) in vascular endothelial cells (EC). PAI‐1 is the physiological inhibitor of tissue and urokinase activators, and a marker of inflammation and endothelial dysfunction. The results of the present study demonstrated that pre‐incubation with gLDL significantly increased the adhesion of THP‐1 monocytes on the surface of cultured human umbilical vein EC (HUVEC) with a peak at 100 μg/ml for 6 h. Transfection of short interference RNA (siRNA) for PAI‐1 to EC prevented gLDL‐induced monocyte adhesion on EC. Scrumble siRNA did not inhibit gLDL‐induced monocyte adhesion on EC. Increased monocyte adhesion on aorta was detected in leptin receptor‐deficient (db/db) diabetic mice. The results of the present study suggest that diabetes‐associated metabolic disorders may promote the adhesion of monocytes to vascular endothelium, and PAI‐1 is required for glyLDL‐induced monocyte adhesion to vascular EC (supported by CDA and CIHR).