SOCS3 promotes apoptosis of mammary differentiated cells

Growth and function of the mammary gland is regulated by cytokines and modulated by suppressor of cytokine signalling (SOCS) proteins. In vitro experiments demonstrated that SOCS3 can inhibit PRL induction of milk protein gene expression and STAT5 activation. We explored the SOCS3 expression pattern...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2005-12, Vol.338 (4), p.1696-1701
Main Authors: Le Provost, Fabienne, Miyoshi, Keiko, Vilotte, Jean-Luc, Bierie, Brian, Robinson, Gertraud W., Hennighausen, Lothar
Format: Article
Language:English
Subjects:
Adipocytes - metabolism
Animals
Apoptosis - drug effects
Cell Differentiation
Differentiation
Epithelial cell
Female
Gene expression
Gene Expression Regulation - drug effects
Growth Hormone - physiology
Involution
JAK/STAT pathway
Lactation - physiology
Life Sciences
Mammary gland
Mammary Glands, Animal - cytology
Mammary Glands, Animal - drug effects
Mice
Prolactin
Prolactin - physiology
STAT5 Transcription Factor - metabolism
Stromal adipocyte
Suppressor of Cytokine Signaling 3 Protein
Suppressor of Cytokine Signaling Proteins - physiology
Suppressor of cytokine signalling
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Summary:Growth and function of the mammary gland is regulated by cytokines and modulated by suppressor of cytokine signalling (SOCS) proteins. In vitro experiments demonstrated that SOCS3 can inhibit PRL induction of milk protein gene expression and STAT5 activation. We explored the SOCS3 expression pattern during mouse mammary development and its regulation by PRL and GH in wild-type and STAT5a-null mammary tissue. Our results suggest that, in vivo, PRL stimulates SOCS3 expression in stromal adipocytes, independently of STAT5a stimulation. In mammary epithelial cells, SOCS3 expression appears to be related to STAT3 activation. Together, our results are consistent with a role of SOCS3 in the mammary gland by promoting apoptosis of differentiated cells (adipocytes during gestation and epithelial cells during involution).
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2005.10.138