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Aldosterone-induced TGF-β(1) Expression is Regulated by Mitogen-Activated Protein Kinases and Activator Protein-1 in Mesangial Cells
Aldosterone has been shown to stimulate renal TGF-β(1) expression. However, the mechanisms for aldosterone-induced TGF-β(1) expression have not been clearly determined in mesangial cells. We examined the role of extracellular-signal regulated kinase 1 and 2 (ERK1/2), c-Jun N-terminal kinase (JNK) an...
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Formato: | Texto |
Lenguaje: | English |
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The Korean Academy of Medical Sciences
2009
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2633178/ https://www.ncbi.nlm.nih.gov/pubmed/19194552 http://dx.doi.org/10.3346/jkms.2009.24.S1.S195 |
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author | Han, Jeong-Sun Choi, Bum-Soon Yang, Chul-Woo Kim, Yong-Soo |
author_facet | Han, Jeong-Sun Choi, Bum-Soon Yang, Chul-Woo Kim, Yong-Soo |
author_sort | Han, Jeong-Sun |
collection | PubMed |
description | Aldosterone has been shown to stimulate renal TGF-β(1) expression. However, the mechanisms for aldosterone-induced TGF-β(1) expression have not been clearly determined in mesangial cells. We examined the role of extracellular-signal regulated kinase 1 and 2 (ERK1/2), c-Jun N-terminal kinase (JNK) and activator protein-1 (AP-1) in the aldosterone-induced TGF-β(1) expression in rat mesangial cells. TGF-β(1) protein in the conditioned medium released from rat mesangial cells was measured by sandwich ELISA, TGF-β(1) mRNA expression was analyzed by Northern blotting, AP-1 DNA binding activity was measured by EMSA and the ERK1/2, JNK activity was analyzed by western blotting. Aldosterone significantly stimulated TGF-β(1) protein production and TGF-β(1) mRNA expression in mesangial cells in a dose-dependent manner. Aldosterone significantly increased AP-1 DNA binding activity in mesangial cells. Pre-treatment of cells with AP-1 inhibitor, curcumin, blocked aldosterone-induced AP-1 DNA binding activity as well as aldosterone-induced TGF-β(1) production. Aldosterone increased phosphorylation of ERK1/2 and JNK in mesangial cells. Pre-treatment of cells with ERK1/2 inhibitor, PD98059, or JNK inhibitor, SP600125 significantly inhibited aldosterone-induced ERK1/2 and JNK activity and subsequently TGF-β(1) production, respectively. We conclude that aldosterone-induced TGF-β(1) expression in mesangial cells is regulated by the ERK1/2, JNK and AP-1 intracellular signaling pathways. |
format | Text |
id | pubmed-2633178 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2009 |
publisher | The Korean Academy of Medical Sciences |
record_format | MEDLINE/PubMed |
spelling | pubmed-26331782009-02-03 Aldosterone-induced TGF-β(1) Expression is Regulated by Mitogen-Activated Protein Kinases and Activator Protein-1 in Mesangial Cells Han, Jeong-Sun Choi, Bum-Soon Yang, Chul-Woo Kim, Yong-Soo J Korean Med Sci Original Article Aldosterone has been shown to stimulate renal TGF-β(1) expression. However, the mechanisms for aldosterone-induced TGF-β(1) expression have not been clearly determined in mesangial cells. We examined the role of extracellular-signal regulated kinase 1 and 2 (ERK1/2), c-Jun N-terminal kinase (JNK) and activator protein-1 (AP-1) in the aldosterone-induced TGF-β(1) expression in rat mesangial cells. TGF-β(1) protein in the conditioned medium released from rat mesangial cells was measured by sandwich ELISA, TGF-β(1) mRNA expression was analyzed by Northern blotting, AP-1 DNA binding activity was measured by EMSA and the ERK1/2, JNK activity was analyzed by western blotting. Aldosterone significantly stimulated TGF-β(1) protein production and TGF-β(1) mRNA expression in mesangial cells in a dose-dependent manner. Aldosterone significantly increased AP-1 DNA binding activity in mesangial cells. Pre-treatment of cells with AP-1 inhibitor, curcumin, blocked aldosterone-induced AP-1 DNA binding activity as well as aldosterone-induced TGF-β(1) production. Aldosterone increased phosphorylation of ERK1/2 and JNK in mesangial cells. Pre-treatment of cells with ERK1/2 inhibitor, PD98059, or JNK inhibitor, SP600125 significantly inhibited aldosterone-induced ERK1/2 and JNK activity and subsequently TGF-β(1) production, respectively. We conclude that aldosterone-induced TGF-β(1) expression in mesangial cells is regulated by the ERK1/2, JNK and AP-1 intracellular signaling pathways. The Korean Academy of Medical Sciences 2009-01 2009-01-28 /pmc/articles/PMC2633178/ /pubmed/19194552 http://dx.doi.org/10.3346/jkms.2009.24.S1.S195 Text en Copyright © 2009 The Korean Academy of Medical Sciences http://creativecommons.org/licenses/by-nc/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Han, Jeong-Sun Choi, Bum-Soon Yang, Chul-Woo Kim, Yong-Soo Aldosterone-induced TGF-β(1) Expression is Regulated by Mitogen-Activated Protein Kinases and Activator Protein-1 in Mesangial Cells |
title | Aldosterone-induced TGF-β(1) Expression is Regulated by Mitogen-Activated Protein Kinases and Activator Protein-1 in Mesangial Cells |
title_full | Aldosterone-induced TGF-β(1) Expression is Regulated by Mitogen-Activated Protein Kinases and Activator Protein-1 in Mesangial Cells |
title_fullStr | Aldosterone-induced TGF-β(1) Expression is Regulated by Mitogen-Activated Protein Kinases and Activator Protein-1 in Mesangial Cells |
title_full_unstemmed | Aldosterone-induced TGF-β(1) Expression is Regulated by Mitogen-Activated Protein Kinases and Activator Protein-1 in Mesangial Cells |
title_short | Aldosterone-induced TGF-β(1) Expression is Regulated by Mitogen-Activated Protein Kinases and Activator Protein-1 in Mesangial Cells |
title_sort | aldosterone-induced tgf-β(1) expression is regulated by mitogen-activated protein kinases and activator protein-1 in mesangial cells |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2633178/ https://www.ncbi.nlm.nih.gov/pubmed/19194552 http://dx.doi.org/10.3346/jkms.2009.24.S1.S195 |
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