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Related Experiment Video

Updated: Sep 27, 2025

Mouse Fetal Liver Culture System to Dissect Target Gene Functions at the Early and Late Stages of Terminal Erythropoiesis

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Published on: September 9, 2014

Constitutively Active STAT5b Feminizes Mouse Liver Gene Expression.

Dana Lau-Corona¹, Hong Ma¹, Cameron Vergato¹

¹Department of Biology and Bioinformatics Program, Boston University, Boston, MA 02215, USA.

|April 9, 2022

Summary

Persistent STAT5 activation in male mouse liver induces feminization by regulating sex-biased genes. This highlights STAT5

Keywords:

JAK-STAT STAT5 knockout liver sex differences pituitary GH secretion profiles

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Last Updated: Sep 27, 2025

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Cell Type-specific Gene Expression Profiling in the Mouse Liver

Cell Type-specific Gene Expression Profiling in the Mouse Liver

Published on: September 17, 2019

Area of Science:

Endocrinology and Molecular Biology
Liver biology and gene regulation

Background:

Growth Hormone (GH) exhibits sex-biased actions in the liver, influencing gene expression differently between males and females.
Signal transducer and activator of transcription 5 (STAT5) is a key regulator mediating these sex-specific GH effects.

Purpose of the Study:

To investigate whether persistent STAT5 activation is sufficient to induce liver feminization in male mice.
To determine the direct role of STAT5 in regulating sex-biased hepatic gene expression.

Main Methods:

Adeno-associated virus (AAV) vector delivery of constitutively active STAT5 (STAT5CA) to male mouse liver.
Analysis of gene expression changes, including induction of female-biased and repression of male-biased genes.
Chromatin immunoprecipitation (ChIP) to identify STAT5 binding sites near responsive genes.

Main Results:

STAT5CA delivery induced widespread liver feminization, mimicking GH-induced effects in males.
STAT5CA significantly altered the expression of numerous sex-biased hepatic genes.
Many STAT5CA-responsive genes were located near STAT5 binding sites, supporting direct transcriptional regulation.
Higher doses of STAT5CA led to dose-dependent feminization and observable histopathology, including hyperplasia and multinuclear hepatocytes.

Conclusions:

Persistent STAT5 activation, as seen in female livers, is sufficient to drive the sex-dependent expression of most hepatic genes.
STAT5CA overexpression demonstrates the critical role of STAT5 in GH-mediated liver feminization.
Potential therapeutic applications of STAT5 derivatives require careful evaluation of associated histopathological risks.