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Evidence in liver for a disulphide-linked scavenger receptor containing a binding site for acetylated low-density lipoprotein and maleylated bovine serum albumin.

ABSTRACT: Membranes from rat liver were analysed under reducing conditions. The components of the soluble membranes responsible for the binding of acetylated low density lipoprotein (acetyl-LDL) and maleylated bovine serum albumin (Mal-BSA) were chromatographed on a polyethyleneimine-cellulose column and subsequently separated by gel electrophoresis. For both ligands a major binding protein (Mr = 35,000) was revealed by ligand blotting. A minor protein (Mr greater than 67,000) exhibited little binding. The Scatchard plot of the 131I-Mal-BSA binding data of the 35 kDa protein was linear, with a Kd of 17.3 nM. High concentrations of acetyl-LDL competed for half of the 131I-Mal-BSA binding. Excessive Mal-BSA competed for all the visible acetyl-LDL binding. The findings indicate the existence, in the reduced hepatic membrane, of a 35 kDa protein that has two binding sites for 131I-Mal-BSA and one binding site for acetyl-LDL.

SUBMITTER: Ottnad E

PROVIDER: S-EPMC1149378 | biostudies-other | 1988 Aug

REPOSITORIES: biostudies-other

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Project description:Thymocyte apoptosis is a major event in sepsis; however, how this process is regulated remains poorly understood.Septic stress induces glucocorticoids production which triggers thymocyte apoptosis. Here, we used scavenger receptor BI (SR-BI)-null mice, which are completely deficient in inducible glucocorticoids in sepsis, to investigate the regulation of thymocyte apoptosis in sepsis. Cecal ligation and puncture induced profound thymocyte apoptosis in SR-BI(+/+) mice, but no thymocyte apoptosis in SR-BI(-/-) mice because of lack of inducible glucocorticoids. Unexpectedly, supplementation of glucocorticoids only partly restored thymocyte apoptosis in SR-BI(-/-) mice. We demonstrated that high-density lipoprotein (HDL) is a critical modulator for thymocyte apoptosis. SR-BI(+/+) HDL significantly enhanced glucocorticoid-induced thymocyte apoptosis, but SR-BI(-/-) HDL had no such activity. Further study revealed that SR-BI(+/+) HDL modulates glucocorticoid-induced thymocyte apoptosis via promoting glucocorticoid receptor translocation, but SR-BI(-/-) HDL loses such regulatory activity. To understand why SR-BI(-/-) HDL loses its regulatory activity, we analyzed HDL cholesterol contents. There was 3-fold enrichment of unesterified cholesterol in SR-BI(-/-) HDL compared with SR-BI(+/+) HDL. Normalization of unesterified cholesterol in SR-BI(-/-) HDL by probucol administration or lecithin cholesteryl acyltransferase expression restored glucocorticoid-induced thymocyte apoptosis, and incorporating unesterified cholesterol into SR-BI(+/+) HDL rendered SR-BI(+/+) HDL dysfunctional. Using lckCre-GR(fl/fl) mice in which thymocytes lack cecal ligation and puncture-induced thymocyte apoptosis, we showed that lckCre-GR(fl/fl) mice were significantly more susceptible to cecal ligation and puncture-induced septic death than GR(fl/fl) control mice, suggesting that glucocorticoid-induced thymocyte apoptosis is required for protection against sepsis.The findings in this study reveal a novel regulatory mechanism of thymocyte apoptosis in sepsis by SR-BI and HDL.

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Evidence in liver for a disulphide-linked scavenger receptor containing a binding site for acetylated low-density lipoprotein and maleylated bovine serum albumin.

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