Modification of human high density lipoprotein by cigarette smoke extract and its impact on reverse cholesterol transport

UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
Chen Chen (Creator)
The University of North Carolina at Greensboro (UNCG )
Web Site:
George Loo

Abstract: High density lipoprotein (HDL) normally functions with lecithin:cholesterol acyltransferase (LCAT) to facilitate reverse cholesterol transport whereby excess cholesterol is removed from peripheral tissue sites, such as arteries. Cigarette smoke contains reactive chemicals which may modify HDL and, therefore, impair its antiatherogenic function in reverse cholesterol transport. We tested this hypothesis by first comparing modification of HDL by cigarette smoke extract (CSE) and acrolein, a potent reactive aldehyde known to be present in cigarette smoke. Both CSE and acrolein caused structural modification of HDL in a concentration-dependent manner, as evidenced by diminution of free amino groups, increase in electrophoretic mobility, and apolipoprotein crosslinking. We then evaluated the capacity of modified HDL to activate LCAT, which requires apolipoprotein A-1 as a cofactor, and also to stimulate cholesterol efflux from THP-1 monocytic cells.

Additional Information

Language: English
Date: 1996
High density lipoproteins
Tobacco $x Physiological effect
Blood cholesterol

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