NDLI: Transcriptional activation by growth hormone of HNF-6-regulated hepatic genes, a potential mechanism for improved liver repair during biliary injury in mice.

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Transcriptional activation by growth hormone of HNF-6-regulated hepatic genes, a potential mechanism for improved liver repair during biliary injury in mice.

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Transcriptional activation by growth hormone of HNF-6-regulated hepatic genes, a potential mechanism for improved liver repair during biliary injury in mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wang, Minhua Chen, Michael Zheng, Guoqiang Dillard, Barney Tallarico, Mike Ortiz, Zorayda Holterman, Ai-Xuan
Description	Country affiliation: United States Author Affiliation: Wang M ( RUSH Univ. Medical Center, Depts. of Pediatrics and Surgery, 1725 W. Harrison St., Suite 718, Chicago, IL, USA.)
Abstract	Growth hormone (GH) function is mediated through multiple endocrine pathways. In the liver, GH also transcriptionally activates hepatocyte nuclear factor-6 (HNF-6; OC-1), a liver-enriched transcription factor that regulates the expression of genes essential to hepatic function. We hypothesize that GH modulates hepatic function in the normal and injured liver through HNF-6 and HNF-6 target genes. CD1 mice received PBS or GH for the 1-, 7-, and 28-day course of Sham operation or bile duct ligation (BDL). Proliferation-, metabolic-, and profibrotic-specific hepatic functions were assessed with a focus on candidate HNF-6 transcriptional target genes. Confirmation of HNF-6 regulation was done by analysis of target gene expression in liver infected with recombinant adenovirus AdHNF-6 expression vectors. GH administration upregulated HNF-6 expression throughout the course of liver injury. This was associated with increased expression of HNF-6 proliferative target genes cyclin D1 and metabolic gene Cyp7A1 and downregulation of profibrogenic TGFb2R. Hepatic function improved such as enhanced hepatocyte proliferation, higher cholesterol clearance throughout the course of injury, and attenuated fibrogenic response at day 28 of BDL. GH treatment also transcriptionally increased albumin expression in an HNF-6-independent manner. This was associated with enhanced serum albumin levels. In conclusion, the GH/HNF-6 axis is a potential in vivo mechanism underlying GH diverse function in the liver to modulate the liver repair response to BDL.
File Format	HTM / HTML
ISSN	01931857
e-ISSN	15221547
DOI	10.1152/ajpgi.00581.2007
Journal	AJP: Gastrointestinal and Liver Physiology
Issue Number	2
Volume Number	295
Language	English
Publisher	American Physiological Society
Publisher Date	2008-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Physiology Discipline Gastroenterology Bile Ducts, Intrahepatic Physiology Cholestasis, Extrahepatic Physiopathology Hepatocyte Nuclear Factor 6 Human Growth Hormone Pharmacology Atp-binding Cassette Transporters Biosynthesis Animals Cell Proliferation Drug Effects Cholesterol 7-alpha-hydroxylase Cyclin D Cyclins Hepatocytes Cytology Ligation Liver Regeneration Mice Organic Anion Transporters, Sodium-dependent Recombinant Proteins Symporters Transcription, Genetic Up-regulation Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Hepatology Physiology Physiology (medical) Gastroenterology

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Transcriptional activation by growth hormone of HNF-6-regulated hepatic genes, a potential mechanism for improved liver repair during biliary injury in mice.

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Transcriptional activation by growth hormone of HNF-6-regulated hepatic genes, a potential mechanism for improved liver repair during biliary injury in mice.