Activation of p53 as a causal step for atherosclerosis induced by polycyclic aromatic hydrocarbons.

Abstract:

:This study was performed to prove our hypothesis that the metabolite(s) of polycyclic aromatic hydrocarbons (PAHs) caused the activation or phosphorylation of p53 via DNA damage to suppress the liver X receptor (LXR)-mediated signal transductions as a probably more direct mechanism. We found that LXR-mediated trans-activation was inhibited by 3-methylchoranthrene (MC) and doxorubicin (Dox) in HepG2 cells carrying wild-type p53, but not in Hep3B cells possessing mutant p53. The exogenous expression of wild-type p53 suppressed the LXR-mediated trans-activation in Hep3B cells. The expression of mRNA for ATP binding cassette A1 was suppressed by MC and Dox in HepG2 cells. The protein expression of retinoid X receptor (RXR), a partner of LXR to form a heterodimer, was suppressed by MC and Dox in HepG2 cells.

journal_name

FEBS Lett

journal_title

FEBS letters

authors

Iwano S,Shibahara N,Saito T,Kamataki T

doi

10.1016/j.febslet.2006.01.009

keywords:

subject

Has Abstract

pub_date

2006-02-06 00:00:00

pages

890-3

issue

3

eissn

0014-5793

issn

1873-3468

pii

S0014-5793(06)00042-1

journal_volume

580

pub_type

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