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.
journal_name
Int J Endocrinoljournal_title
International journal of endocrinologyauthors
Song K,Han Y,Zhang L,Liu G,Yang P,Cheng X,Bu L,Sheng H,Qu Sdoi
10.1155/2014/356432subject
Has Abstractpub_date
2014-01-01 00:00:00pages
356432eissn
1687-8337issn
1687-8345journal_volume
2014pub_type
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journal_title:International journal of endocrinology
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journal_title:International journal of endocrinology
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