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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

Multiplicity of infection (MOI) test in HepG2 cells and primary hepatocytes. HepG2 cells (a) and the isolated primary hepatocytes were pretreated with Ad-ATPase-B1 and Ad-GFP with different MOIs, and ATPase-B1 mRNA (b) and protein ((c) A, ATPase-B1 expression in WT primary hepatocytes; B, ATPase-B1 expression in SR-BI−/− primary hepatocytes; C, the internal control of GADPH in WT and SR-BI−/− primary hepatocytes) levels were measured. In HepG2 cells and WT hepatocytes, mRNA expression increased with increased MOI, while mRNA expression peaked at 30 MOIs in SR-BI−/− mouse.
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fig3: Multiplicity of infection (MOI) test in HepG2 cells and primary hepatocytes. HepG2 cells (a) and the isolated primary hepatocytes were pretreated with Ad-ATPase-B1 and Ad-GFP with different MOIs, and ATPase-B1 mRNA (b) and protein ((c) A, ATPase-B1 expression in WT primary hepatocytes; B, ATPase-B1 expression in SR-BI−/− primary hepatocytes; C, the internal control of GADPH in WT and SR-BI−/− primary hepatocytes) levels were measured. In HepG2 cells and WT hepatocytes, mRNA expression increased with increased MOI, while mRNA expression peaked at 30 MOIs in SR-BI−/− mouse.

Mentions: To further investigate how different quantities of ATPase-B1 affect its cellular expression, we infected HepG2 cells with various concentrations of Ad-ATPase-B1 and Ad-GFP. Increased MOI corresponded to increased ATPase-B1 protein (Figure 3(a)) and mRNA expression (data not shown).


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)

Multiplicity of infection (MOI) test in HepG2 cells and primary hepatocytes. HepG2 cells (a) and the isolated primary hepatocytes were pretreated with Ad-ATPase-B1 and Ad-GFP with different MOIs, and ATPase-B1 mRNA (b) and protein ((c) A, ATPase-B1 expression in WT primary hepatocytes; B, ATPase-B1 expression in SR-BI−/− primary hepatocytes; C, the internal control of GADPH in WT and SR-BI−/− primary hepatocytes) levels were measured. In HepG2 cells and WT hepatocytes, mRNA expression increased with increased MOI, while mRNA expression peaked at 30 MOIs in SR-BI−/− mouse.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig3: Multiplicity of infection (MOI) test in HepG2 cells and primary hepatocytes. HepG2 cells (a) and the isolated primary hepatocytes were pretreated with Ad-ATPase-B1 and Ad-GFP with different MOIs, and ATPase-B1 mRNA (b) and protein ((c) A, ATPase-B1 expression in WT primary hepatocytes; B, ATPase-B1 expression in SR-BI−/− primary hepatocytes; C, the internal control of GADPH in WT and SR-BI−/− primary hepatocytes) levels were measured. In HepG2 cells and WT hepatocytes, mRNA expression increased with increased MOI, while mRNA expression peaked at 30 MOIs in SR-BI−/− mouse.
Mentions: To further investigate how different quantities of ATPase-B1 affect its cellular expression, we infected HepG2 cells with various concentrations of Ad-ATPase-B1 and Ad-GFP. Increased MOI corresponded to increased ATPase-B1 protein (Figure 3(a)) and mRNA expression (data not shown).

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