ATP Synthase β-Chain Overexpression in SR-BI Knockout Mice Increases HDL Uptake and Reduces Plasma HDL Level. (10th July 2014)

• Record Type: Journal Article
• Authors: Song, Kexiu; Han, Yingchun; Zhang, Linhua; Liu, Guoqing; Yang, Peng; Cheng, Xiaoyun; Bu, Le; Sheng, Hui; Qu, Shen
• Other Names: Russo Giuseppina T. Academic Editor.
• Is Part Of: International journal of endocrinology. Volume 2014(2014)
• Publication Date: 2014-07-10
• Subjects: Endocrinology -- Periodicals; Endocrinology; Endocrinology -- Periodicals; Endocrine System Diseases -- Periodicals; Periodicals; 616.4
• DOI: 10.1155/2014/356432
• Languages: English
• ISSNs: 1687-8337

Abstract

Abstract : HDL cholesterol is known to be inversely correlated with cardiovascular disease due to its diverse antiatherogenic functions. SR-BI mediates the selective uptake of HDL-C. SR-BI knockout diminishes but does not completely block the transport of HDL; other receptors may be involved. Ectopic ATP synthase β -chain in hepatocytes has been previously characterized as an apoA-I receptor, triggering HDL internalization. This study was undertaken to identify the overexpression of ectopic ATP synthase β -chain on DIL-HDL uptake in primary hepatocytes in vitro and on plasma HDL levels in SR-BI knockout mice. Human ATP synthase β -chain cDNA was delivered to the mouse liver by adenovirus and GFP adenovirus as control. The adenovirus-mediated overexpression of β -chain was identified at both mRNA and protein levels on mice liver and validated by its increasing of DiL-HDL uptake in primary hepatocytes. In response to hepatic overexpression of β -chain, plasma HDL-C levels and cholesterol were reduced in SR-BI knockout mice, compared with the control. The present data suggest that ATP synthase β -chain can serve as the endocytic receptor of HDL, and its overexpression can reduce plasma HDL-C.