Glucocorticoid alternative effects on proliferating and differentiated mammary epithelium are associated to opposite regulation of cell-cycle inhibitor expression

Glucocorticoids influence post-natal mammary gland development by sequentially controlling cell proliferation, differentiation, and apoptosis. In the mammary gland, it has been demonstrated that glucocorticoid treatment inhibits epithelial apoptosis in post-lactating glands. In this study, our first...

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Autores principales:	Hoijman, Esteban, Rocha Viegas, Luciana, Kalko, Susana G., Rubinstein, Natalia, Kordon, Edith Claudia, Pecci, Adali
Publicado:	2012
Materias:	ATM protein caspase 3 CRADD protein cyclin dependent kinase inhibitor 1 cyclin dependent kinase inhibitor 2C dexamethasone animal cell animal experiment animal tissue apoptosis article breast epithelium cell cycle regulation cell differentiation cell proliferation cell survival controlled study down regulation female gene expression gene expression profiling gene overexpression lactation mammary gland microarray analysis mouse nonhuman nucleotide sequence priority journal regulatory mechanism Animals Cell Cycle Cell Cycle Proteins Cell Differentiation Cell Proliferation Cyclin-Dependent Kinase Inhibitor p18 Cyclin-Dependent Kinase Inhibitor p21 Dexamethasone DNA-Binding Proteins Epithelial Cells Female Gene Expression Regulation, Developmental Glucocorticoids Lactation Mammary Glands, Animal Mice Mice, Inbred BALB C Protein-Serine-Threonine Kinases Tumor Suppressor Proteins
Acceso en línea:	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00219541_v227_n4_p1721_Hoijman http://hdl.handle.net/20.500.12110/paper_00219541_v227_n4_p1721_Hoijman
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

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spelling	paper:paper_00219541_v227_n4_p1721_Hoijman2023-06-08T14:43:48Z Glucocorticoid alternative effects on proliferating and differentiated mammary epithelium are associated to opposite regulation of cell-cycle inhibitor expression Hoijman, Esteban Rocha Viegas, Luciana Kalko, Susana G. Rubinstein, Natalia Kordon, Edith Claudia Pecci, Adali ATM protein caspase 3 CRADD protein cyclin dependent kinase inhibitor 1 cyclin dependent kinase inhibitor 2C dexamethasone animal cell animal experiment animal tissue apoptosis article breast epithelium cell cycle regulation cell differentiation cell proliferation cell survival controlled study down regulation female gene expression gene expression profiling gene overexpression lactation mammary gland microarray analysis mouse nonhuman nucleotide sequence priority journal regulatory mechanism Animals Cell Cycle Cell Cycle Proteins Cell Differentiation Cell Proliferation Cyclin-Dependent Kinase Inhibitor p18 Cyclin-Dependent Kinase Inhibitor p21 Dexamethasone DNA-Binding Proteins Epithelial Cells Female Gene Expression Regulation, Developmental Glucocorticoids Lactation Mammary Glands, Animal Mice Mice, Inbred BALB C Protein-Serine-Threonine Kinases Tumor Suppressor Proteins Glucocorticoids influence post-natal mammary gland development by sequentially controlling cell proliferation, differentiation, and apoptosis. In the mammary gland, it has been demonstrated that glucocorticoid treatment inhibits epithelial apoptosis in post-lactating glands. In this study, our first goal was to identify new glucocorticoid target genes that could be involved in generating this effect. Expression profiling, by microarray analysis, revealed that expression of several cell-cycle control genes was altered by dexamethasone (DEX) treatment after lactation. Importantly, it was determined that not only the exogenous synthetic hormone, but also the endogenous glucocorticoids regulated the expression of these genes. Particularly, we found that the expression of cell cycle inhibitors p21CIP1, p18INK4c, and Atm was differentially regulated by glucocorticoids through the successive stages of mammary gland development. In undifferentiated cells, DEX treatment induced their expression and reduced cell proliferation, while in differentiated cells this hormone repressed expression of those cell cycle inhibitors and promoted survival. Therefore, differentiation status determined the effect of glucocorticoids on mammary cell fate. Particularly, we have determined that p21CIP1 inhibition would mediate the activity of these hormones in differentiated mammary cells because over-expression of this protein blocked DEX-induced apoptosis protection. Together, our data suggest that the multiple roles played by glucocorticoids in mammary gland development and function might be at least partially due to the alternative roles that these hormones play on the expression of cell cycle regulators. © 2011 Wiley Periodicals, Inc. Fil:Hoijman, E. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Rocha-Viegas, L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Kalko, S.G. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Rubinstein, N. 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. 2012 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00219541_v227_n4_p1721_Hoijman http://hdl.handle.net/20.500.12110/paper_00219541_v227_n4_p1721_Hoijman
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	ATM protein caspase 3 CRADD protein cyclin dependent kinase inhibitor 1 cyclin dependent kinase inhibitor 2C dexamethasone animal cell animal experiment animal tissue apoptosis article breast epithelium cell cycle regulation cell differentiation cell proliferation cell survival controlled study down regulation female gene expression gene expression profiling gene overexpression lactation mammary gland microarray analysis mouse nonhuman nucleotide sequence priority journal regulatory mechanism Animals Cell Cycle Cell Cycle Proteins Cell Differentiation Cell Proliferation Cyclin-Dependent Kinase Inhibitor p18 Cyclin-Dependent Kinase Inhibitor p21 Dexamethasone DNA-Binding Proteins Epithelial Cells Female Gene Expression Regulation, Developmental Glucocorticoids Lactation Mammary Glands, Animal Mice Mice, Inbred BALB C Protein-Serine-Threonine Kinases Tumor Suppressor Proteins
spellingShingle	ATM protein caspase 3 CRADD protein cyclin dependent kinase inhibitor 1 cyclin dependent kinase inhibitor 2C dexamethasone animal cell animal experiment animal tissue apoptosis article breast epithelium cell cycle regulation cell differentiation cell proliferation cell survival controlled study down regulation female gene expression gene expression profiling gene overexpression lactation mammary gland microarray analysis mouse nonhuman nucleotide sequence priority journal regulatory mechanism Animals Cell Cycle Cell Cycle Proteins Cell Differentiation Cell Proliferation Cyclin-Dependent Kinase Inhibitor p18 Cyclin-Dependent Kinase Inhibitor p21 Dexamethasone DNA-Binding Proteins Epithelial Cells Female Gene Expression Regulation, Developmental Glucocorticoids Lactation Mammary Glands, Animal Mice Mice, Inbred BALB C Protein-Serine-Threonine Kinases Tumor Suppressor Proteins Hoijman, Esteban Rocha Viegas, Luciana Kalko, Susana G. Rubinstein, Natalia Kordon, Edith Claudia Pecci, Adali Glucocorticoid alternative effects on proliferating and differentiated mammary epithelium are associated to opposite regulation of cell-cycle inhibitor expression
topic_facet	ATM protein caspase 3 CRADD protein cyclin dependent kinase inhibitor 1 cyclin dependent kinase inhibitor 2C dexamethasone animal cell animal experiment animal tissue apoptosis article breast epithelium cell cycle regulation cell differentiation cell proliferation cell survival controlled study down regulation female gene expression gene expression profiling gene overexpression lactation mammary gland microarray analysis mouse nonhuman nucleotide sequence priority journal regulatory mechanism Animals Cell Cycle Cell Cycle Proteins Cell Differentiation Cell Proliferation Cyclin-Dependent Kinase Inhibitor p18 Cyclin-Dependent Kinase Inhibitor p21 Dexamethasone DNA-Binding Proteins Epithelial Cells Female Gene Expression Regulation, Developmental Glucocorticoids Lactation Mammary Glands, Animal Mice Mice, Inbred BALB C Protein-Serine-Threonine Kinases Tumor Suppressor Proteins
description	Glucocorticoids influence post-natal mammary gland development by sequentially controlling cell proliferation, differentiation, and apoptosis. In the mammary gland, it has been demonstrated that glucocorticoid treatment inhibits epithelial apoptosis in post-lactating glands. In this study, our first goal was to identify new glucocorticoid target genes that could be involved in generating this effect. Expression profiling, by microarray analysis, revealed that expression of several cell-cycle control genes was altered by dexamethasone (DEX) treatment after lactation. Importantly, it was determined that not only the exogenous synthetic hormone, but also the endogenous glucocorticoids regulated the expression of these genes. Particularly, we found that the expression of cell cycle inhibitors p21CIP1, p18INK4c, and Atm was differentially regulated by glucocorticoids through the successive stages of mammary gland development. In undifferentiated cells, DEX treatment induced their expression and reduced cell proliferation, while in differentiated cells this hormone repressed expression of those cell cycle inhibitors and promoted survival. Therefore, differentiation status determined the effect of glucocorticoids on mammary cell fate. Particularly, we have determined that p21CIP1 inhibition would mediate the activity of these hormones in differentiated mammary cells because over-expression of this protein blocked DEX-induced apoptosis protection. Together, our data suggest that the multiple roles played by glucocorticoids in mammary gland development and function might be at least partially due to the alternative roles that these hormones play on the expression of cell cycle regulators. © 2011 Wiley Periodicals, Inc.
author	Hoijman, Esteban Rocha Viegas, Luciana Kalko, Susana G. Rubinstein, Natalia Kordon, Edith Claudia Pecci, Adali
author_facet	Hoijman, Esteban Rocha Viegas, Luciana Kalko, Susana G. Rubinstein, Natalia Kordon, Edith Claudia Pecci, Adali
author_sort	Hoijman, Esteban
title	Glucocorticoid alternative effects on proliferating and differentiated mammary epithelium are associated to opposite regulation of cell-cycle inhibitor expression
title_short	Glucocorticoid alternative effects on proliferating and differentiated mammary epithelium are associated to opposite regulation of cell-cycle inhibitor expression
title_full	Glucocorticoid alternative effects on proliferating and differentiated mammary epithelium are associated to opposite regulation of cell-cycle inhibitor expression
title_fullStr	Glucocorticoid alternative effects on proliferating and differentiated mammary epithelium are associated to opposite regulation of cell-cycle inhibitor expression
title_full_unstemmed	Glucocorticoid alternative effects on proliferating and differentiated mammary epithelium are associated to opposite regulation of cell-cycle inhibitor expression
title_sort	glucocorticoid alternative effects on proliferating and differentiated mammary epithelium are associated to opposite regulation of cell-cycle inhibitor expression
publishDate	2012
url	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00219541_v227_n4_p1721_Hoijman http://hdl.handle.net/20.500.12110/paper_00219541_v227_n4_p1721_Hoijman
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_version_	1768543931274887168

Glucocorticoid alternative effects on proliferating and differentiated mammary epithelium are associated to opposite regulation of cell-cycle inhibitor expression

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