NDLI: Loss of Sexually Dimorphic Liver Gene Expression Upon Hepatocyte-specific Deletion of Stat5a-Stat5b Locus

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Loss of Sexually Dimorphic Liver Gene Expression Upon Hepatocyte-specific Deletion of Stat5a-Stat5b Locus

Content Provider	PubMed Central
Author	Holloway, Minita G. Cui, Yongzhi Laz, Ekaterina Atsushi, Hosui Hennighausen, Lothar Waxman, David J.
Abstract	Hepatocyte-specific, albumin-Cre recombinase-mediated deletion of the entire mouse Stat5a-Stat5b locus was carried out to evaluate the role of STAT5a and STAT5b (STAT5ab) in the sex-dependent transcriptional actions of GH in the liver. The resultant hepatocyte STAT5ab-deficient mice were fertile, and unlike global STAT5b-deficient male mice, postnatal body weight gain was normal, despite a 50% decrease in serum IGF1. Whole liver STAT5ab RNA decreased by ∼65-85%, and residual STAT5 immunostaining was observed in a minority of the hepatocytes, indicating incomplete excision by Cre-recombinase. Quantitative PCR analysis of twenty sexually dimorphic, liver-expressed genes revealed significant down-regulation of 10 of 11 male-specific genes in livers of male hepatocyte STAT5ab-deficient mice. Class I female-specific liver genes (Holloway et al (2006) Molec Endocrinol 20: 647-660) were markedly up regulated (de-repressed), whereas the expression of class II female genes, belonging to the Cyp3a subfamily, was unaffected by the loss of hepatocyte STAT5ab. STAT5ab is thus required in the liver for positive regulation of male-specific genes and for negative regulation of a subset of female-specific genes. Continuous GH infusion strongly induced (>500-fold) the class II female gene Cyp3a16 in both wild type and hepatocyte STAT5ab-deficient male mice, indicating sex-specific transcriptional regulation by GH that is STAT5ab-independent. In contrast, hepatocyte STAT5ab deficiency abolished the strong suppression of the male-specific Cyp2d9 by continuous GH seen in control mouse liver. Analysis of global STAT5a-deficient mice indicated no essential requirement of STAT5a for expression of these sex-specific liver Cyp genes. Thus, the major loss of liver sexual dimorphism in hepatocyte STAT5ab-deficient mice can primarily be attributed to the loss of STAT5b.
Related Links	http://dx.doi.org/10.1210/en.2006-1419
Ending Page	1986
Page Count	10
Starting Page	1977
File Format	PDF
ISSN	00137227
e-ISSN	19457170
Journal	Endocrinology
Issue Number	5
Volume Number	148
Language	English
Publisher Date	2007-05-01
Access Restriction	Open
Subject Keyword	Endocrinology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Endocrinology

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