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Sterol-regulatory-element binding protein inhibits upstream stimulatory factor-stimulated hepatic lipase gene expression.

Abstract：

:Hepatic lipase (HL) not only plays an important role in plasma lipoprotein transport, but may also affect intracellular lipid metabolism. We hypothesize that HL expression is regulated as an integral part of intracellular lipid homeostasis. Addition of oleate (1 mM) to HepG2 cells increased HL secretion to 134+/-14% of control (p<0.02), and increased the transcriptional activity of a 698-bp HL promoter-reporter construct two-fold. Atorvastatin (10 microM) abolished the oleate stimulation. The transcriptional activity of a sterol-regulatory-element binding protein (SREBP)-sensitive HMG-CoA synthase promoter construct was reduced 50% by oleate, and increased 2-3-fold by atorvastatin. Co-transfection with an SREBP-2 expression vector reduced HL promoter activity and increased HMG-CoA synthase promoter activity. Upstream stimulatory factors (USF) are also implicated in maintenance of lipid homeostasis. Co-transfection with a USF-1 expression vector stimulated HL promoter activity 4-6-fold. The USF-stimulated HL promoter activity was not further enhanced by oleate, but almost completely prevented by atorvastatin or co-transfection with the SREBP-2 vector. Opposite regulation by USF-1 and SREBP-2 was also observed with a 318-bp HL promoter construct that lacks potential SRE-like and E-box binding motifs. We conclude that the opposite regulation of HL expression by fatty acids and statins is mediated via SREBP, possibly through interaction with USF.

journal_name

Atherosclerosis

journal_title

Atherosclerosis

authors

Botma GJ,van Deursen D,Vieira D,van Hoek M,Jansen H,Verhoeven AJ

doi

10.1016/j.atherosclerosis.2004.10.027

keywords:

subject

Has Abstract

pub_date

2005-03-01 00:00:00

pages

61-7

issue

1

eissn

0021-9150

issn

1879-1484

pii

S0021-9150(04)00564-7

journal_volume

179

pub_type

杂志文章

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