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Aromatic residues in the C terminus of apolipoprotein C-III mediate lipid binding and LPL inhibition
Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Fysiologisk kemi.
Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Fysiologisk kemi.
Vise andre og tillknytning
2017 (engelsk)Inngår i: JOURNAL OF LIPID RESEARCH, Vol. 58, nr 5, s. 840-852Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Plasma apoC-III levels correlate with triglyceride (TG) levels and are a strong predictor of CVD outcomes. ApoC-III elevates TG in part by inhibiting LPL. ApoC-III likely inhibits LPL by competing for lipid binding. To probe this, we used oil-drop tensiometry to characterize binding of six apoC-III variants to lipid/water interfaces. This technique monitors the dependence of lipid binding on surface pressure, which increases during TG hydrolysis by LPL. ApoC-III adsorption increased surface pressure by upward of 18 mN/m at phospholipid/TG/water interfaces. ApoC-III was retained to high pressures at these interfaces, desorbing at 21-25 mN/m. Point mutants, which substituted alanine for aromatic residues, impaired the lipid binding of apoC-III. Adsorption and retention pressures decreased by 1-6 mN/m in point mutants, with the magnitude determined by the location of alanine substitutions. Trp42 was most critical to mediating lipid binding. These results strongly correlate with our previous results, linking apoC-III point mutants to increased LPL binding and activity at lipid surfaces.(jlr) We propose that aromatic residues in the C-terminal half of apoC-III mediate binding to TG-rich lipoproteins. Increased apoC-III expression in the hypertriglyceridemic state allows apoC-III to accumulate on lipoproteins and inhibit LPL by preventing binding and/or access to sub-strate.

sted, utgiver, år, opplag, sider
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC , 2017. Vol. 58, nr 5, s. 840-852
Emneord [en]
lipoprotein lipase, lipid and lipoprotein metabolism, LDL/metabolism, lipid/emulsions, protein-lipid teraction, surface pressure, drop tensiometry
HSV kategori
Identifikatorer
URN: urn:nbn:se:umu:diva-136199DOI: 10.1194/jlr.M071126ISI: 000400479800004PubMedID: 28159869OAI: oai:DiVA.org:umu-136199DiVA, id: diva2:1120727
Tilgjengelig fra: 2017-07-07 Laget: 2017-07-07 Sist oppdatert: 2018-06-09bibliografisk kontrollert

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