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Urotensin II increases foam cell formation by repressing ABCA1 expression through the ERK/NF-κB pathway in THP-1 macrophages.

Abstract：

OBJECTIVE:Foam cell formation in the arterial wall plays a key role in the development of atherosclerosis. Recent studies showed that Urotensin II (U II) is involved in the pathogenesis of atherosclerosis. Here we examined the effects of human U II on ATP-binding cassette transporter A1 (ABCA1) expression and the underlying mechanism in THP-1 macrophages. METHODS AND RESULTS:Cultured THP-1 macrophages were treated with U II, followed by measuring the intracellular lipid contents, cholesterol efflux and ABCA1 levels. The results showed that U II dramatically decreased ABCA1 levels and impaired cholesterol efflux. However, the effects of U II on ABCA1 protein expression and cellular cholesterol efflux were partially reversed by inhibition of extracellular signal regulated kinase 1/2 (ERK1/2) and nuclear factor kappa B (NF-κB) activity, suggesting the potential roles of ERK1/2 and NF-κB in ABCA1 expression, respectively. CONCLUSION:Our current data indicate that U II may have promoting effects on the progression of atherosclerosis, likely through suppressing ABCA1 expression via activation of the ERK/NF-κB pathway and reducing cholesterol efflux to promote macrophage foam cell formation.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Wang Y,Wu JF,Tang YY,Zhang M,Li Y,Chen K,Zeng MY,Yao F,Xie W,Zheng XL,Zeng GF,Tang CK

doi

10.1016/j.bbrc.2014.09.030

subject

Has Abstract

pub_date

2014-10-03 00:00:00

pages

998-1003

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(14)01638-6

journal_volume

452

pub_type

杂志文章

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