Involvement of KLF14 and egr-1 in the TGF-beta1 action on Leydig cell proliferation
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...
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2013
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10434666_v61_n2_p670_Gonzalez http://hdl.handle.net/20.500.12110/paper_10434666_v61_n2_p670_Gonzalez |
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paper:paper_10434666_v61_n2_p670_Gonzalez2023-06-08T16:01:01Z Involvement of KLF14 and egr-1 in the TGF-beta1 action on Leydig cell proliferation 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 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. 2013 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10434666_v61_n2_p670_Gonzalez http://hdl.handle.net/20.500.12110/paper_10434666_v61_n2_p670_Gonzalez |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
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 |
| spellingShingle |
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 Involvement of KLF14 and egr-1 in the TGF-beta1 action on Leydig cell proliferation |
| topic_facet |
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 |
| description |
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. |
| title |
Involvement of KLF14 and egr-1 in the TGF-beta1 action on Leydig cell proliferation |
| title_short |
Involvement of KLF14 and egr-1 in the TGF-beta1 action on Leydig cell proliferation |
| title_full |
Involvement of KLF14 and egr-1 in the TGF-beta1 action on Leydig cell proliferation |
| title_fullStr |
Involvement of KLF14 and egr-1 in the TGF-beta1 action on Leydig cell proliferation |
| title_full_unstemmed |
Involvement of KLF14 and egr-1 in the TGF-beta1 action on Leydig cell proliferation |
| title_sort |
involvement of klf14 and egr-1 in the tgf-beta1 action on leydig cell proliferation |
| publishDate |
2013 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10434666_v61_n2_p670_Gonzalez http://hdl.handle.net/20.500.12110/paper_10434666_v61_n2_p670_Gonzalez |
| _version_ |
1768543956344242176 |