Characterization of peroxisome proliferator-activated receptor alpha--independent effects of PPARalpha activators in the rodent liver: di-(2-ethylhexyl) phthalate also activates the constitutive-activated receptor

Ren, H; Aleksunes, L; Wood, C; Vallanat, B; George, M; Klaassen, C; Corton, J

HERO ID

697411

Reference Type

Journal Article

Year

2010

Language

English

PMID

19850644

HERO ID 697411
In Press No
Year 2010
Title Characterization of peroxisome proliferator-activated receptor alpha--independent effects of PPARalpha activators in the rodent liver: di-(2-ethylhexyl) phthalate also activates the constitutive-activated receptor
Authors Ren, H; Aleksunes, L; Wood, C; Vallanat, B; George, M; Klaassen, C; Corton, J
Journal Toxicological Sciences
Volume 113
Issue 1
Page Numbers 45-59
Abstract Peroxisome proliferator chemicals (PPC) are thought to mediate their effects in rodents on hepatocyte growth and liver cancer through the nuclear receptor peroxisome proliferator-activated receptor (PPAR) alpha. Recent studies indicate that the plasticizer di-(2-ethylhexyl) phthalate (DEHP) increased the incidence of liver tumors in PPARalpha-null mice. We hypothesized that some PPC, including DEHP, induce transcriptional changes independent of PPARalpha but dependent on other nuclear receptors, including the constitutive-activated receptor (CAR) that mediates phenobarbital (PB) effects on hepatocyte growth and liver tumor induction. To determine the potential role of CAR in mediating effects of PPC, a meta-analysis was performed on transcript profiles from published studies in which rats and mice were exposed to PPC and compared the profiles to those produced by exposure to PB. Valproic acid, clofibrate, and DEHP in rat liver and DEHP in mouse liver induced genes, including Cyp2b family members that are known to be regulated by CAR. Examination of transcript changes by Affymetrix ST 1.0 arrays and reverse transcription-PCR in the livers of DEHP-treated wild-type, PPARalpha-null, and CAR-null mice demonstrated that (1) most (approximately 94%) of the transcriptional changes induced by DEHP were PPARalpha-dependent, (2) many PPARalpha-independent genes overlapped with those regulated by PB, (3) induction of genes Cyp2b10, Cyp3a11, and metallothionine-1 by DEHP was CAR dependent but PPARalpha-independent, and (4) induction of a number of genes (Cyp8b1, Gstm4, and Gstm7) was independent of both CAR and PPARalpha. Our results indicate that exposure to PPARalpha activators including DEHP leads to activation of multiple nuclear receptors in the rodent liver.
Doi 10.1093/toxsci/kfp251
Pmid 19850644
Wosid WOS:000272935700005
Url https://www.scopus.com/inward/record.uri?eid=2-s2.0-75249083175&doi=10.1093%2ftoxsci%2fkfp251&partnerID=40&md5=ef426d258ecb93f081c8b884e5d001a8
Is Certified Translation No
Dupe Override No
Comments Source: Web of Science WOS:000272935700005
Is Public Yes
Language Text English
Keyword peroxisome proliferator-activated receptor alpha; transcript profiling; liver cancer; di-(2-ethylhexyl) phthalate; constitutive-activated receptor; pregnane X receptor
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