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Interaction of discoidal complexes of dimyristoyl phosphatidylcholine‐cholesterol‐apolipoprotein A‐I with human plasma high density lipoprotein HDL 3
Author(s) -
Jackson Richard L.,
Cardin Alan D.,
Barnhart Roger L.,
Ashraf Muhammad,
Johnson J. David
Publication year - 1982
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02535191
Subject(s) - lipidology , clinical chemistry , apolipoprotein b , high density lipoprotein , cholesterol , phosphatidylcholine , human plasma , apolipoprotein c2 , lipoprotein , low density lipoprotein receptor related protein 8 , apolipoprotein a1 , chemistry , intermediate density lipoprotein , plasma , very low density lipoprotein , biochemistry , phospholipid , chromatography , membrane , physics , quantum mechanics
The interaction of human plasma high density lipoproteins (HDL 3 ) with discoidal complexes of apolipoprotein A‐I (apoA‐I) and dimyristoyl phosphatidylcholine (DMPC) containing 0, 10, 20 or 30 mol % cholesterol was investigated. Discoidal complexes containing various amounts of cholesterol were prepared by incubating apoA‐I and DMPC‐cholesterol liposomes for 12 hr at 25 C; the protein‐lipid complexes were isolated by gel filtration chromatography on Bio‐Gel A15m. Increasing the cholesterol content from 0 to 30 mol % caused a decrease in the fluidity of the discoidal complexes as determined by fluorescence polarization with 1,6‐diphenyl‐1,3,5‐hexatriene; a reduced phase‐transition amplitude; a decrease in the ratio of apoA‐I to DMPC; and an increase in the width of the discoidal complexes as determined by electron microscopy after negative staining. Incubation of the apoA‐I‐lipid complexes with HDL 3 resulted in a complete breakdown of the discoidal structures and a transfer of DMPC and cholesterol to HDL 3 . As a result of lipid transfer, there was an increase in the size of HDL 3 . These in vitro results may be of significance as they relate to the interconversion of HDL subfractions during lipoprotein‐lipase‐induced lipolysis of triglyceride‐rich lipoproteins.