Artículo

Hoijman, E.; Rocha-Viegas, L.; Kalko, S.G.; Rubinstein, N.; Morales-Ruiz, M.; de Kier Joffé, E.B.; Kordon, E.C.; Pecci, A. "Glucocorticoid alternative effects on proliferating and differentiated mammary epithelium are associated to opposite regulation of cell-cycle inhibitor expression" (2012) Journal of Cellular Physiology. 227(4):1721-1730
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Abstract:

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.

Registro:

Documento: Artículo
Título:Glucocorticoid alternative effects on proliferating and differentiated mammary epithelium are associated to opposite regulation of cell-cycle inhibitor expression
Autor:Hoijman, E.; Rocha-Viegas, L.; Kalko, S.G.; Rubinstein, N.; Morales-Ruiz, M.; de Kier Joffé, E.B.; Kordon, E.C.; Pecci, A.
Filiación:IFIBYNE-CONICET, Buenos Aires, Argentina
Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina
Departamento de Fisiología y Biología Molecular y Celular, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina
Unidad de Bioinformática, Hospital Clinic, IDIBAPS, Barcelona, Spain
Departamento de Bioquímica y Genética Molecular, Hospital Clinic, IDIBAPS, Barcelona, Spain
Area Investigación Instituto de Oncología Ángel H. Roffo, Universidad de Buenos Aires, Buenos Aires, Argentina
Palabras clave: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
Año:2012
Volumen:227
Número:4
Página de inicio:1721
Página de fin:1730
DOI: http://dx.doi.org/10.1002/jcp.22896
Título revista:Journal of Cellular Physiology
Título revista abreviado:J. Cell. Physiol.
ISSN:00219541
CODEN:JCLLA
CAS:caspase 3, 169592-56-7; dexamethasone, 50-02-2; Cdkn1a protein, mouse; Cdkn2c protein, mouse; Cell Cycle Proteins; Cyclin-Dependent Kinase Inhibitor p18; Cyclin-Dependent Kinase Inhibitor p21; DNA-Binding Proteins; Dexamethasone, 50-02-2; Glucocorticoids; Protein-Serine-Threonine Kinases, 2.7.11.1; Tumor Suppressor Proteins; ataxia telangiectasia mutated protein, 2.7.11.1
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00219541_v227_n4_p1721_Hoijman

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Citas:

---------- APA ----------
Hoijman, E., Rocha-Viegas, L., Kalko, S.G., Rubinstein, N., Morales-Ruiz, M., de Kier Joffé, E.B., Kordon, E.C.,..., Pecci, A. (2012) . Glucocorticoid alternative effects on proliferating and differentiated mammary epithelium are associated to opposite regulation of cell-cycle inhibitor expression. Journal of Cellular Physiology, 227(4), 1721-1730.
http://dx.doi.org/10.1002/jcp.22896
---------- CHICAGO ----------
Hoijman, E., Rocha-Viegas, L., Kalko, S.G., Rubinstein, N., Morales-Ruiz, M., de Kier Joffé, E.B., et al. "Glucocorticoid alternative effects on proliferating and differentiated mammary epithelium are associated to opposite regulation of cell-cycle inhibitor expression" . Journal of Cellular Physiology 227, no. 4 (2012) : 1721-1730.
http://dx.doi.org/10.1002/jcp.22896
---------- MLA ----------
Hoijman, E., Rocha-Viegas, L., Kalko, S.G., Rubinstein, N., Morales-Ruiz, M., de Kier Joffé, E.B., et al. "Glucocorticoid alternative effects on proliferating and differentiated mammary epithelium are associated to opposite regulation of cell-cycle inhibitor expression" . Journal of Cellular Physiology, vol. 227, no. 4, 2012, pp. 1721-1730.
http://dx.doi.org/10.1002/jcp.22896
---------- VANCOUVER ----------
Hoijman, E., Rocha-Viegas, L., Kalko, S.G., Rubinstein, N., Morales-Ruiz, M., de Kier Joffé, E.B., et al. Glucocorticoid alternative effects on proliferating and differentiated mammary epithelium are associated to opposite regulation of cell-cycle inhibitor expression. J. Cell. Physiol. 2012;227(4):1721-1730.
http://dx.doi.org/10.1002/jcp.22896