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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003849naa a2200505 4500
001oai:DiVA.org:kth-16332
003SwePub
008100805s2007 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:13919220
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-163322 URI
0247 a https://doi.org/10.1124/jpet.106.1132092 DOI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:139192202 URI
040 a (SwePub)kthd (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Henriquez-Hernandez, L. A.4 aut
2451 0a Role of pituitary hormones on 17 alpha-ethinylestradiol-induced cholestasis in rat
264 c 2006-11-15
264 1b American Society for Pharmacology & Experimental Therapeutics (ASPET),c 2007
338 a print2 rdacarrier
500 a QC 20100525
520 a Estrogens cause intrahepatic cholestasis in susceptible women during pregnancy, after administration of oral contraceptives, or during postmenopausal hormone replacement therapy. 17 alpha-Ethinylestradiol ( EE) is a synthetic estrogen widely used to cause experimental cholestasis in rodents with the aim of examining molecular mechanisms involved in this disease. EE actions on the liver are thought to be mediated by estrogen receptor alpha ( ER alpha) and pituitary hormones. We tested this hypothesis by analyzing metabolic changes induced by EE in livers from hypophysectomized ( HYPOX) and hypothyroid rats. Microarray studies revealed that the number of genes regulated by EE was increased almost 4-fold in HYPOX rat livers compared with intact males. Little overlap was apparent between the effects of EE in intact and HYPOX rats, demonstrating that pituitary hormones play a critical role in the hepatic effects of EE. Consistently, hypophysectomy protects the liver against induction by EE of serum bilirubin and alkaline phosphatase, two markers of cholestasis and hepatotoxicity and modulates the effects of EE on several genes involved in bile acid homeostasis ( e. g., FXR, SHP, BSEP, and Cyp8b1). Finally, we demonstrate a novel mechanism of action of EE through binding and negative regulation of glucocorticoid receptor-mediated transcription. In summary, pituitary- and ER alpha- independent mechanisms contribute to development of EE-induced changes in liver transcriptome. Such mechanisms may be relevant when this model of EE-induced cholestasis is evaluated. The observation that the pharmacological effects of estrogen in liver differ in the absence or presence of the pituitary could be clinically relevant, because different drugs that block actions of pituitary hormones are now available.
653 a small heterodimer partner
653 a growth-hormone
653 a gene-expression
653 a in-vivo
653 a cholesterol 7-alpha-hydroxylase
653 a estrogen-receptor
653 a bile-acids
653 a sterol 12-alpha-hydroxylase
653 a microarray data
653 a target genes
7001 a Flores-Morales, A.u Karolinska Institutet4 aut
7001 a Santana-Farre, R.4 aut
7001 a Axelson, M.4 aut
7001 a Nilsson, Peteru KTH,Proteomik4 aut0 (Swepub:kth)u1ws88sk
7001 a Norstedt, G.u Karolinska Institutet4 aut
7001 a Fernandez-Perez, L.4 aut
7102 a Karolinska Institutetb Proteomik4 org
7730 t Journal of Pharmacology and Experimental Therapeuticsd : American Society for Pharmacology & Experimental Therapeutics (ASPET)g 320:2, s. 695-705q 320:2<695-705x 0022-3565x 1521-0103
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-16332
8564 8u https://doi.org/10.1124/jpet.106.113209
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:13919220

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