Yazarlar : Orsoni A, Villard EF, Bruckert E et al

Yayın : J Lipid Res.

Pubmed Linki : http://www.ncbi.nlm.nih.gov/pubmed/22338009

Konu : Aferez

Literatür İçeriği :  

Abstract

Background: In Familial Hypercholesterolemia (FH) low HDL-C levels are associated with functional alterations of HDL particles that reduce their capacity to mediate the reverse cholesterol transport (RCT) pathway. The objective of this study was to evaluate the consequences of LDL apheresison the efficacy of the RCT pathway in FH patients.Methods and Results: LDL apheresis markedly reduced abnormal accelerated CETP-mediated CE transfer from HDL to LDL, thus reducing their CE content. Equally we observed a major decrease (-53%;p<0.0001) in prebeta1-HDL levels. The capacity of whole plasma to mediate FC efflux from human macrophages was reduced (-15%;p<0.02) following LDL apheresis. Such reduction resulted from a marked decrease in the ABCA1-dependent efflux (-71%;p<0.0001), in the SR-BI dependent efflux (-21%;p<0.0001) and in the ABCG1-dependent pathway (-15%;p<0.04). However, HDL particles isolated from FH patients before and after LDL apheresis displayed a similar capacity to mediate cellular FC efflux or to deliver CE to hepatic cells.Conclusion: We demonstrate that rapid removal of circulating lipoprotein particles by LDLapheresis transitory reduces RCT. However, LDL apheresis is without impact on the intrinsic ability of HDL particles to promote either cellular free efflux cholesterol from macrophages or to deliver CE to hepatic cells.

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