Glucocorticoid-induced impairment of mammary gland involution is associated with STAT5 and STAT3 signaling modulation

The mammary epithelium undergoes cyclical periods of cellular proliferation, differentiation, and regression. During lactation, the signal transducer and activator of transcription factor (STAT)-5A and the glucocorticoid receptor (GR) synergize to induce milk protein expression and also act as survi...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Bertucci, Paola Yanina, Quaglino, Ana, Pozzi, Andrea Gabriela, Kordon, Edith Claudia, Pecci, Adali
Publicado:	2010
Materias:	beta casein dexamethasone glucocorticoid prolactin STAT3 protein STAT5 protein animal experiment animal tissue apoptosis article down regulation epithelium cell extracellular matrix gene expression mammary gland mouse nonhuman priority journal protein degradation signal transduction weaning Animals Cytokine Receptor gp130 Dexamethasone DNA Fragmentation Female Gene Expression Regulation Glucocorticoids Lactation Leukemia Inhibitory Factor Mammary Glands, Animal Mice Mice, Inbred BALB C Signal Transduction STAT3 Transcription Factor STAT5 Transcription Factor
Acceso en línea:	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00137227_v151_n12_p5730_Bertucci http://hdl.handle.net/20.500.12110/paper_00137227_v151_n12_p5730_Bertucci
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

id	paper:paper_00137227_v151_n12_p5730_Bertucci
record_format	dspace
spelling	paper:paper_00137227_v151_n12_p5730_Bertucci2023-06-08T14:36:14Z Glucocorticoid-induced impairment of mammary gland involution is associated with STAT5 and STAT3 signaling modulation Bertucci, Paola Yanina Quaglino, Ana Pozzi, Andrea Gabriela Kordon, Edith Claudia Pecci, Adali beta casein dexamethasone glucocorticoid prolactin STAT3 protein STAT5 protein animal experiment animal tissue apoptosis article down regulation epithelium cell extracellular matrix gene expression mammary gland mouse nonhuman priority journal protein degradation signal transduction weaning Animals Cytokine Receptor gp130 Dexamethasone DNA Fragmentation Female Gene Expression Regulation Glucocorticoids Lactation Leukemia Inhibitory Factor Mammary Glands, Animal Mice Mice, Inbred BALB C Signal Transduction STAT3 Transcription Factor STAT5 Transcription Factor The mammary epithelium undergoes cyclical periods of cellular proliferation, differentiation, and regression. During lactation, the signal transducer and activator of transcription factor (STAT)-5A and the glucocorticoid receptor (GR) synergize to induce milk protein expression and also act as survival factors. During involution, STAT3 activation mediates epithelial cell apoptosis and mammary gland remodeling. It has been shown that the administration of glucocorticoids at weaning prevents epithelial cell death, probably by extracellular matrix breakdown prevention. Our results show that the synthetic glucocorticoid dexamethasone (DEX) modulates STAT5A and STAT3 signaling and inhibits apoptosis induction in postlactating mouse mammary glands, only when administered within the first 48 h upon cessation of suckling. DEX administration right after weaning delayed STAT5A inactivation and degradation, preserving gene expression of target genes as β-casein (bcas) and prolactin induced protein (pip). Weaning-triggered GR down-regulation is also delayed by the hormone treatment. Moreover, DEX administration delayed STAT3 activation and translocation into epithelial cells nuclei. In particular, DEX treatment impaired the increment in gene expression of signal transducer subunit gp130, normally up-regulated from lactation to involution and responsible for STAT3 activation. Therefore, the data shown herein indicate that glucocorticoids are able to modulate early involution by controlling the strong cross talk that GR, STAT5, and STAT3 pathways maintains in the mammary epithelium. Copyright © 2010 by The Endocrine Society. Fil:Bertucci, P.Y. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Quaglino, A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Pozzi, A.G. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Kordon, E.C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Pecci, A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2010 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00137227_v151_n12_p5730_Bertucci http://hdl.handle.net/20.500.12110/paper_00137227_v151_n12_p5730_Bertucci
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	beta casein dexamethasone glucocorticoid prolactin STAT3 protein STAT5 protein animal experiment animal tissue apoptosis article down regulation epithelium cell extracellular matrix gene expression mammary gland mouse nonhuman priority journal protein degradation signal transduction weaning Animals Cytokine Receptor gp130 Dexamethasone DNA Fragmentation Female Gene Expression Regulation Glucocorticoids Lactation Leukemia Inhibitory Factor Mammary Glands, Animal Mice Mice, Inbred BALB C Signal Transduction STAT3 Transcription Factor STAT5 Transcription Factor
spellingShingle	beta casein dexamethasone glucocorticoid prolactin STAT3 protein STAT5 protein animal experiment animal tissue apoptosis article down regulation epithelium cell extracellular matrix gene expression mammary gland mouse nonhuman priority journal protein degradation signal transduction weaning Animals Cytokine Receptor gp130 Dexamethasone DNA Fragmentation Female Gene Expression Regulation Glucocorticoids Lactation Leukemia Inhibitory Factor Mammary Glands, Animal Mice Mice, Inbred BALB C Signal Transduction STAT3 Transcription Factor STAT5 Transcription Factor Bertucci, Paola Yanina Quaglino, Ana Pozzi, Andrea Gabriela Kordon, Edith Claudia Pecci, Adali Glucocorticoid-induced impairment of mammary gland involution is associated with STAT5 and STAT3 signaling modulation
topic_facet	beta casein dexamethasone glucocorticoid prolactin STAT3 protein STAT5 protein animal experiment animal tissue apoptosis article down regulation epithelium cell extracellular matrix gene expression mammary gland mouse nonhuman priority journal protein degradation signal transduction weaning Animals Cytokine Receptor gp130 Dexamethasone DNA Fragmentation Female Gene Expression Regulation Glucocorticoids Lactation Leukemia Inhibitory Factor Mammary Glands, Animal Mice Mice, Inbred BALB C Signal Transduction STAT3 Transcription Factor STAT5 Transcription Factor
description	The mammary epithelium undergoes cyclical periods of cellular proliferation, differentiation, and regression. During lactation, the signal transducer and activator of transcription factor (STAT)-5A and the glucocorticoid receptor (GR) synergize to induce milk protein expression and also act as survival factors. During involution, STAT3 activation mediates epithelial cell apoptosis and mammary gland remodeling. It has been shown that the administration of glucocorticoids at weaning prevents epithelial cell death, probably by extracellular matrix breakdown prevention. Our results show that the synthetic glucocorticoid dexamethasone (DEX) modulates STAT5A and STAT3 signaling and inhibits apoptosis induction in postlactating mouse mammary glands, only when administered within the first 48 h upon cessation of suckling. DEX administration right after weaning delayed STAT5A inactivation and degradation, preserving gene expression of target genes as β-casein (bcas) and prolactin induced protein (pip). Weaning-triggered GR down-regulation is also delayed by the hormone treatment. Moreover, DEX administration delayed STAT3 activation and translocation into epithelial cells nuclei. In particular, DEX treatment impaired the increment in gene expression of signal transducer subunit gp130, normally up-regulated from lactation to involution and responsible for STAT3 activation. Therefore, the data shown herein indicate that glucocorticoids are able to modulate early involution by controlling the strong cross talk that GR, STAT5, and STAT3 pathways maintains in the mammary epithelium. Copyright © 2010 by The Endocrine Society.
author	Bertucci, Paola Yanina Quaglino, Ana Pozzi, Andrea Gabriela Kordon, Edith Claudia Pecci, Adali
author_facet	Bertucci, Paola Yanina Quaglino, Ana Pozzi, Andrea Gabriela Kordon, Edith Claudia Pecci, Adali
author_sort	Bertucci, Paola Yanina
title	Glucocorticoid-induced impairment of mammary gland involution is associated with STAT5 and STAT3 signaling modulation
title_short	Glucocorticoid-induced impairment of mammary gland involution is associated with STAT5 and STAT3 signaling modulation
title_full	Glucocorticoid-induced impairment of mammary gland involution is associated with STAT5 and STAT3 signaling modulation
title_fullStr	Glucocorticoid-induced impairment of mammary gland involution is associated with STAT5 and STAT3 signaling modulation
title_full_unstemmed	Glucocorticoid-induced impairment of mammary gland involution is associated with STAT5 and STAT3 signaling modulation
title_sort	glucocorticoid-induced impairment of mammary gland involution is associated with stat5 and stat3 signaling modulation
publishDate	2010
url	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00137227_v151_n12_p5730_Bertucci http://hdl.handle.net/20.500.12110/paper_00137227_v151_n12_p5730_Bertucci
work_keys_str_mv	AT bertuccipaolayanina glucocorticoidinducedimpairmentofmammaryglandinvolutionisassociatedwithstat5andstat3signalingmodulation AT quaglinoana glucocorticoidinducedimpairmentofmammaryglandinvolutionisassociatedwithstat5andstat3signalingmodulation AT pozziandreagabriela glucocorticoidinducedimpairmentofmammaryglandinvolutionisassociatedwithstat5andstat3signalingmodulation AT kordonedithclaudia glucocorticoidinducedimpairmentofmammaryglandinvolutionisassociatedwithstat5andstat3signalingmodulation AT pecciadali glucocorticoidinducedimpairmentofmammaryglandinvolutionisassociatedwithstat5andstat3signalingmodulation
_version_	1768543639011590144

Glucocorticoid-induced impairment of mammary gland involution is associated with STAT5 and STAT3 signaling modulation

Ejemplares similares