高α脂蛋白血症患者人巨噬细胞的血浆胆固醇外排能力增强。
Improved plasma cholesterol efflux capacity from human macrophages in patients with hyperalphalipoproteinemia.
机构信息
INSERM-UPMC UMR1166, Hôpital de la Pitié, Paris, France; Laboratoire de Biochimie, Faculté de Pharmacie et Pôle Technologie Santé, Université Saint-Joseph, Beirut, Lebanon.
Hormonal and Metabolic Disorders Research Unit and Endocrinology and Metabolism Unit, Department of Medecine, Faculty of Medicine, Chulalongkorn University and King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Patumwan, Bangkok, Thailand.
出版信息
Atherosclerosis. 2014 May;234(1):193-9. doi: 10.1016/j.atherosclerosis.2014.02.032. Epub 2014 Mar 12.
OBJECTIVES
CETP or HL deficiencies lead to a marked increase in HDL-C levels however the atheroprotective effect of this phenotype, in particular the ability of HDL particles to remove cholesterol from human macrophages, remains to be determined.
METHODS
We measured cholesterol efflux from human THP-1 macrophages to total plasma or to isolated HDL subfractions in patients with HALP carrying molecular defect in either the CETP or LIPC gene.
RESULTS
We demonstrate that HALP is associated with an increased plasma cholesterol efflux capacity from human macrophages. This observation is primarily related to a stimulation of both SR-BI and ABCA1 dependent efflux pathways as a result of quantitative elevation in HDL2 and enhanced intrinsic capacity of HDL3 subspecies, respectively.
CONCLUSION
HDL particles from HALP patients with molecular defect within either CETP or LIPC gene are not dysfunctional and are efficient to stimulate cholesterol efflux from human macrophages.
目的
CETP 或 HL 缺乏会导致 HDL-C 水平显著升高，但这种表型的抗动脉粥样硬化作用，特别是 HDL 颗粒从人巨噬细胞中去除胆固醇的能力，仍有待确定。
方法
我们测量了携带 CETP 或 LIPC 基因突变的 HALP 患者的总血浆或分离的 HDL 亚组分中胆固醇从人 THP-1 巨噬细胞的流出情况。
结果
我们证明 HALP 与人类巨噬细胞中血浆胆固醇流出能力的增加有关。这一观察结果主要与 HDL2 的定量升高以及 HDL3 亚种内在能力的增强分别导致 SR-BI 和 ABCA1 依赖性流出途径的刺激有关。
结论
在 CETP 或 LIPC 基因内具有分子缺陷的 HALP 患者的 HDL 颗粒没有功能障碍，能够有效地刺激人巨噬细胞中的胆固醇流出。
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