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ATP Synthase β-Chain Overexpression in SR-BI Knockout Mice Increases HDL Uptake and Reduces Plasma HDL Level.

Song K, Han Y, Zhang L, Liu G, Yang P, Cheng X, Bu L, Sheng H, Qu S - Int J Endocrinol (2014)

Bottom Line: HDL cholesterol is known to be inversely correlated with cardiovascular disease due to its diverse antiatherogenic functions.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Endocrinology, Shanghai Tenth People's Hospital, Tongji University, 301 Middle Yanchang Road, Shanghai 200072, China.

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.

No MeSH data available.


Related in: MedlinePlus

Plasma triglyceride (a), total cholesterol (b), and HDL-C (c) levels in WT and SR-BI−/− mice 7 days after administration of Ad-ATPase-B1 and Ad-GFP.
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fig7: Plasma triglyceride (a), total cholesterol (b), and HDL-C (c) levels in WT and SR-BI−/− mice 7 days after administration of Ad-ATPase-B1 and Ad-GFP.

Mentions: Plasma total cholesterol and HDL-C were 2.5 and 3 times higher, respectively, in SR-BI−/− mice before infection (Figures 6(a)–6(c)). SR-BI−/− mice infected with Ad-ATPase-B1 showed lower plasma total cholesterol (~18%) and HDL-C (~12%) compared to SR-BI−/− mice infected with the control adenovirus (Figures 7(a)-7(b)), but plasma triglycerides were not different between the groups (Figure 7(c)). ATPase-B1 infection did not affect plasma total cholesterol, HDL-C, or triglycerides in WT mice (Figures 7(a)–7(c)). Analysis of lipoprotein profiles in the pooled plasma sample revealed lower HDL-cholesterol (Figure 8) in the Ad-ATPase-B1 mice compared to Ad-GFP mice. However, Ad-ATPase-B1 treated mice showed a significant increase in VLDL/CM-associated TG compared to Ad-GFP mice (Figure 8(a)).


ATP Synthase β-Chain Overexpression in SR-BI Knockout Mice Increases HDL Uptake and Reduces Plasma HDL Level.

Song K, Han Y, Zhang L, Liu G, Yang P, Cheng X, Bu L, Sheng H, Qu S - Int J Endocrinol (2014)

Plasma triglyceride (a), total cholesterol (b), and HDL-C (c) levels in WT and SR-BI−/− mice 7 days after administration of Ad-ATPase-B1 and Ad-GFP.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4120797&req=5

fig7: Plasma triglyceride (a), total cholesterol (b), and HDL-C (c) levels in WT and SR-BI−/− mice 7 days after administration of Ad-ATPase-B1 and Ad-GFP.
Mentions: Plasma total cholesterol and HDL-C were 2.5 and 3 times higher, respectively, in SR-BI−/− mice before infection (Figures 6(a)–6(c)). SR-BI−/− mice infected with Ad-ATPase-B1 showed lower plasma total cholesterol (~18%) and HDL-C (~12%) compared to SR-BI−/− mice infected with the control adenovirus (Figures 7(a)-7(b)), but plasma triglycerides were not different between the groups (Figure 7(c)). ATPase-B1 infection did not affect plasma total cholesterol, HDL-C, or triglycerides in WT mice (Figures 7(a)–7(c)). Analysis of lipoprotein profiles in the pooled plasma sample revealed lower HDL-cholesterol (Figure 8) in the Ad-ATPase-B1 mice compared to Ad-GFP mice. However, Ad-ATPase-B1 treated mice showed a significant increase in VLDL/CM-associated TG compared to Ad-GFP mice (Figure 8(a)).

Bottom Line: HDL cholesterol is known to be inversely correlated with cardiovascular disease due to its diverse antiatherogenic functions.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Endocrinology, Shanghai Tenth People's Hospital, Tongji University, 301 Middle Yanchang Road, Shanghai 200072, China.

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.

No MeSH data available.


Related in: MedlinePlus