Apolipoprotein A-I carboxy-terminal domain residues 187-243 are required for adiponectin-induced cholesterol efflux. Cell Signal 2022 Mar;91:110222
Date
12/27/2021Pubmed ID
34954016DOI
10.1016/j.cellsig.2021.110222Scopus ID
2-s2.0-85121847439 (requires institutional sign-in at Scopus site)Abstract
Adiponectin exerts its atheroprotection by stimulating adenosine triphosphate binding cassette transporter A1 (ABCA1)-mediated cholesterol efflux to apolipoprotein A-I (apoA-I). However, involvement of the apoA-I residues in this process have not been studied. In Tamm-Horsfall 1 (THP-1) macrophages and baby hamster kidney (BHK) cells we assessed adiponectin's potential to restore cholesterol efflux in the presence of apoA-I and ABCA1 mutants, respectively. Adiponectin was unable to restore efflux from THP-1 macrophages in the presence of apoA-I carboxy-terminal domain (CTD) successive mutants from residues 187-243 versus apoA-I mutants alone. Furthermore, adiponectin did not significantly influence cholesterol efflux to apoA-I from BHK-ABCA1 mutant cells. Adiponectin appears to require functional apoA-I CTD residues 187-243 and wild-type ABCA1 to mediate efficient cholesterol efflux from THP-1 macrophages and BHK cells, respectively. Therefore, adiponectin cannot rescue defective cholesterol efflux in apoA-I- or ABCA1-mutant conditions, but rather increases cholesterol efflux in wild-type apoA-I conditions compared to apoA-I exposure alone.
Author List
Hafiane A, Gianopoulos I, Sorci-Thomas MG, Daskalopoulou SSAuthor
Mary Sorci Thomas PhD Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
ATP Binding Cassette Transporter 1ATP-Binding Cassette Transporters
Adiponectin
Animals
Apolipoprotein A-I
Cell Line
Cholesterol
Cricetinae
Humans
THP-1 Cells
