| Aldosterone stimulates proliferation of mesangial cells by activating mitogen-activated protein kinase 1/2, cyclin D1, and cyclin A. | |
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MedLine Citation:
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PMID: 15975997 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Recently, attention has been focused on the role of aldosterone in the pathophysiology of hypertension and cardiovascular disease. Several clinical and experimental data support the hypothesis that aldosterone contributes to the progression of renal injury. However, the molecular mechanisms of the effects of aldosterone in signal transduction and the cell-cycle progression of mesangial cells are not well known. For determining the signaling pathway of aldosterone in cultured mesangial cells, the effects of aldosterone on the mitogen-activated protein kinase 1/2 (MAPK1/2) pathway and the promoter activities of cyclin D1, cyclin A, and cyclin E were investigated. First, it was shown that the mineralocorticoid receptor (MR) was expressed in rat mesangial cells and glomeruli and that aldosterone stimulated the proliferation of mesangial cells via the MR and MAPK1/2 pathway. Next, it was demonstrated that aldosterone stimulated Ki-RasA, c-Raf kinase, MEK1/2, and MAPK1/2 in rat mesangial cells. Aldosterone induced cyclin D1 and cyclin A promoter activities and protein expressions, as well as the increments of CDK2 and CDK4 kinase activities. The presence of CYP11B2 and 11beta-HSD2 mRNA in rat mesangial cells also was shown. In conclusion, aldosterone seems to exert mainly MR-induced effects that stimulate c-Raf, MEK1/2, MAPK1/2, the activities of CDK2 and CDK4, and the cell-cycle progression in mesangial cells. MR antagonists may serve as a potential therapeutic approach to mesangial proliferative disease. |
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Authors:
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Yoshio Terada; Takahiko Kobayashi; Hitoshi Kuwana; Hiroyuki Tanaka; Seiji Inoshita; Michio Kuwahara; Sei Sasaki |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2005-06-23 |
Journal Detail:
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Title: Journal of the American Society of Nephrology : JASN Volume: 16 ISSN: 1046-6673 ISO Abbreviation: J. Am. Soc. Nephrol. Publication Date: 2005 Aug |
Date Detail:
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Created Date: 2005-07-21 Completed Date: 2006-02-03 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 9013836 Medline TA: J Am Soc Nephrol Country: United States |
Other Details:
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Languages: eng Pagination: 2296-305 Citation Subset: IM |
Affiliation:
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Department of Nephrology, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8519, Japan. yterada.kid@tmd.ac.jp |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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11-beta-Hydroxysteroid Dehydrogenase Type 2
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metabolism Aldosterone / metabolism, pharmacology* Aldosterone Synthase / metabolism Animals Blotting, Western Cell Cycle Cell Proliferation Cyclin A / genetics, metabolism* Cyclin D1 / genetics, metabolism* Cyclin E / genetics Disease Progression Flow Cytometry Genes, Reporter Kidney / cytology, injuries, pathology Kidney Cortex / metabolism Kidney Glomerulus / metabolism Luciferases / metabolism MAP Kinase Signaling System Male Mesangial Cells / metabolism*, pathology Mitogen-Activated Protein Kinase 1 / metabolism* Mitogen-Activated Protein Kinase 3 / metabolism* Promoter Regions, Genetic Proto-Oncogene Proteins / chemistry Proto-Oncogene Proteins c-raf / metabolism Rats Rats, Sprague-Dawley Receptors, Mineralocorticoid / biosynthesis Reverse Transcriptase Polymerase Chain Reaction Thymidine / metabolism Time Factors Transfection ras Proteins |
| Chemical | |
Reg. No./Substance:
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0/Cyclin A; 0/Cyclin E; 0/KRAS protein, human; 0/Proto-Oncogene Proteins; 0/Receptors, Mineralocorticoid; 136601-57-5/Cyclin D1; 50-89-5/Thymidine; 52-39-1/Aldosterone; EC 1.1.1.146/11-beta-Hydroxysteroid Dehydrogenase Type 2; EC 1.13.12.-/Luciferases; EC 1.14.15.4/Aldosterone Synthase; EC 2.7.11.1/Proto-Oncogene Proteins c-raf; EC 2.7.11.24/Mitogen-Activated Protein Kinase 1; EC 2.7.11.24/Mitogen-Activated Protein Kinase 3; EC 3.6.5.2/ras Proteins |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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