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Abstract:

Transforming growth factor β1 (TGF-β1) is a pleiotropic cytokine that modulates cell homeostasis. In Leydig cells, TGF-β1 exerts stimulatory and inhibitory effect depending on the type I receptor involved in the signaling pathway. The aim of the present work was to study the signaling mechanisms and the intermediates involved in the action of TGF-β1 on TM3 Leydig cell proliferation in the presence or absence of progesterone. The MTT assay showed that the presence of progesterone in the culture media lead to a proliferative effect that was blocked by Ru 486, an inhibitor of progesterone receptor; and ALK-5 did not participate in this effect. TGF-β1 (1. ng/ml) increased the expression of p15 (an inhibitor of cell cycle) in TM3 Leydig cells, and this effect was blocked by progesterone (1 μM). The expression of PCNA presented a higher increase in the cell cultured with TGF-β1 plus progesterone than in cells cultured only with TGF-β1.Progesterone induced the gene expression of endoglin, a cofactor of TGF-β1 receptor that leads to a stimulatory signaling pathway, despite of the absence of progesterone response element in endoglin gene. In addition, the presence of progesterone induced the gene expression of egr-1 and also KLF14, indicating that this steroid channels the signaling pathway into a non-canonical mechanism. In conclusion, these findings suggest that the proliferative action of TGF-β1 involves endoglin. This co-receptor might be induced by KLF14 which is probably activated by progesterone. © 2012 Elsevier Ltd.

Registro:

Documento: Artículo
Título:Involvement of KLF14 and egr-1 in the TGF-beta1 action on Leydig cell proliferation
Autor:Gonzalez, C.R.; Vallcaneras, S.S.; Calandra, R.S.; Gonzalez Calvar, S.I.
Filiación:Research Center of Biomedical Biotechnology, Environmental and Diagnostic Studies, Maimónides University, Hidalgo 775, 1405 Buenos Aires, Argentina
Laboratory of Biology of Reproduction, School of Chemistry, Biochemistry and Pharmacy, National University of San Luis, Ejército de los Andes 950, 5700 San Luis, Argentina
Institute of Biology and Experimental Medicine, National Council for Scientific and Technical Research, Vuelta de Obligado 2490, 1428 Buenos Aires, Argentina
School of Medicine, Buenos Aires University, 2155, 1121 Buenos Aires, Argentina
Palabras clave:KLF14; Leydig cells; Proliferation; TGF-β1; cycline; early growth response factor 1; endoglin; kruppel like factor; kruppel like factor 14; mifepristone; progesterone; protein p15; transforming growth factor beta receptor 1; transforming growth factor beta1; unclassified drug; animal cell; article; cell assay; cell culture; cell cycle; cell proliferation; controlled study; culture medium; gene expression; Leydig cell; mouse; nonhuman; nucleotide sequence; priority journal; protein expression; signal transduction; Activin Receptors, Type I; Animals; Cell Line; Cell Proliferation; Cyclin-Dependent Kinase Inhibitor p15; DNA, Complementary; Early Growth Response Protein 1; Gene Expression Regulation; Humans; Intracellular Signaling Peptides and Proteins; Kruppel-Like Transcription Factors; Leydig Cells; Male; Mice; Mice, Inbred BALB C; Progesterone; Proliferating Cell Nuclear Antigen; Protein-Serine-Threonine Kinases; Real-Time Polymerase Chain Reaction; Receptors, Transforming Growth Factor beta; Response Elements; Transcription Factors; Transforming Growth Factor beta1
Año:2013
Volumen:61
Número:2
Página de inicio:670
Página de fin:675
DOI: http://dx.doi.org/10.1016/j.cyto.2012.12.009
Título revista:Cytokine
Título revista abreviado:Cytokine
ISSN:10434666
CODEN:CYTIE
CAS:mifepristone, 84371-65-3; progesterone, 57-83-0; Activin Receptors, Type I, 2.7.11.30; Acvrl1 protein, mouse, 2.7.11.30; Cyclin-Dependent Kinase Inhibitor p15; DNA, Complementary; Early Growth Response Protein 1; Egr1 protein, mouse; Intracellular Signaling Peptides and Proteins; Klf14 protein, mouse; Kruppel-Like Transcription Factors; Progesterone, 57-83-0; Proliferating Cell Nuclear Antigen; Protein-Serine-Threonine Kinases, 2.7.11.1; Receptors, Transforming Growth Factor beta; TGF-beta type I receptor, 2.7.1.11; Tgfb1 protein, mouse; Transcription Factors; Transforming Growth Factor beta1; endoglin protein, mouse; transforming growth factor-beta type II receptor, 2.7.11.30
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10434666_v61_n2_p670_Gonzalez

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Citas:

---------- APA ----------
Gonzalez, C.R., Vallcaneras, S.S., Calandra, R.S. & Gonzalez Calvar, S.I. (2013) . Involvement of KLF14 and egr-1 in the TGF-beta1 action on Leydig cell proliferation. Cytokine, 61(2), 670-675.
http://dx.doi.org/10.1016/j.cyto.2012.12.009
---------- CHICAGO ----------
Gonzalez, C.R., Vallcaneras, S.S., Calandra, R.S., Gonzalez Calvar, S.I. "Involvement of KLF14 and egr-1 in the TGF-beta1 action on Leydig cell proliferation" . Cytokine 61, no. 2 (2013) : 670-675.
http://dx.doi.org/10.1016/j.cyto.2012.12.009
---------- MLA ----------
Gonzalez, C.R., Vallcaneras, S.S., Calandra, R.S., Gonzalez Calvar, S.I. "Involvement of KLF14 and egr-1 in the TGF-beta1 action on Leydig cell proliferation" . Cytokine, vol. 61, no. 2, 2013, pp. 670-675.
http://dx.doi.org/10.1016/j.cyto.2012.12.009
---------- VANCOUVER ----------
Gonzalez, C.R., Vallcaneras, S.S., Calandra, R.S., Gonzalez Calvar, S.I. Involvement of KLF14 and egr-1 in the TGF-beta1 action on Leydig cell proliferation. Cytokine. 2013;61(2):670-675.
http://dx.doi.org/10.1016/j.cyto.2012.12.009