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Titolo:
Effects of ursodeoxycholic and cholic acid feeding on hepatocellular transporter expression in mouse liver
Autore:
Fickert, P; Zollner, G; Fuchsbichler, A; Stumptner, C; Pojer, C; Zenz, R; Lammert, F; Stieger, B; Meier, PJ; Zatloukal, K; Denk, H; Trauner, M;
Indirizzi:
Karl Franzens Univ Graz, Dept Med, Div Gastroenterol & Hepatol, A-8036 Graz, Austria Karl Franzens Univ Graz Graz Austria A-8036 epatol, A-8036 Graz, Austria Karl Franzens Univ Graz, Dept Pathol, A-8036 Graz, Austria Karl Franzens Univ Graz Graz Austria A-8036 Pathol, A-8036 Graz, Austria Univ Aachen, Dept Med, Aachen, Germany Univ Aachen Aachen GermanyUniv Aachen, Dept Med, Aachen, Germany Univ Zurich Hosp, Dept Med, Div Clin Pharmacol & Toxicol, CH-8091 Zurich, Switzerland Univ Zurich Hosp Zurich Switzerland CH-8091 CH-8091 Zurich, Switzerland
Titolo Testata:
GASTROENTEROLOGY
fascicolo: 1, volume: 121, anno: 2001,
pagine: 170 - 183
SICI:
0016-5085(200107)121:1<170:EOUACA>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLYCOPROTEIN-DEFICIENT MICE; TRANSCRIPT TITRATION ASSAY; MULTIDRUG-RESISTANCE GENE; PRIMARY BILIARY-CIRRHOSIS; SALT EXPORT PUMP; RAT-LIVER; P-GLYCOPROTEIN; BILE-ACIDS; MOLECULAR-CLONING; MESSENGER-RNA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
67
Recensione:
Indirizzi per estratti:
Indirizzo: Trauner, M Karl Franzens Univ Graz, Dept Med, Div Gastroenterol & Hepatol,Auenbruggerpl 15, A-8036 Graz, Austria Karl Franzens Univ Graz Auenbruggerpl 15 Graz Austria A-8036 a
Citazione:
P. Fickert et al., "Effects of ursodeoxycholic and cholic acid feeding on hepatocellular transporter expression in mouse liver", GASTROENTY, 121(1), 2001, pp. 170-183

Abstract

Background & Aims: Cholestasis is associated with retention of potentiallytoxic bile acids and alterations in hepatocellular transporter expression. Conversely, nontoxic ursodeoxycholic acid (UDCA) stimulates bile secretionand counteracts cholestasis. This study aimed to determine the effects of UDCA and cholic acid (CA) on the expression of hepatocellular transporters for bile acids (Ntcp, Bsep), organic anions (Oatp1, Mrp2), organic cations (Mdr1a/b), and phospholipids (Mdr2) in mouse liver. Methods: Bile flow/composition was analyzed in UDCA- or CA-fed mice. Transporter expression was studied by reverse-transcription polymerase chain reaction, Western blotting,and immunofluorescence microscopy. Results: UDCA had no effect on basolateral Ntcp and down-regulated Oatp1, whereas canalicular Bsep and Mrp2 were up-regulated. CA down-regulated basolateral Ntcp and Oatp1, whereas canalicular Bsep, Mrp2, and Mdr1a/b were up-regulated. Neither UDCA nor CA affectedMdr2 expression. Both UDCA and CA stimulated biliary bile acid and glutathione excretion, although only CA increased phospholipid and cholesterol excretion. Conclusions: Down-regulation of basolateral and up-regulation of canalicular transporters in response to CA may represent a defense mechanism,in an attempt to prevent hepatocellular accumulation of potentially toxic bile acids. The therapeutic effects of UDCA may be caused in part by stimulation of canalicular transporter expression in the absence of hepatocellular toxicity.

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Documento generato il 07/07/20 alle ore 21:44:57