Aldosterone Regulates Cellular Turnover and Mitogen-Activated Protein Kinase Family Expression in the Neonatal Rat Kidney
DC Field | Value | Language |
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dc.contributor.author | Yim, Hyung Eun | - |
dc.contributor.author | Yoo, Kee Hwan | - |
dc.contributor.author | Bae, In Sun | - |
dc.contributor.author | Jang, Gi Young | - |
dc.contributor.author | Hong, Young Sook | - |
dc.contributor.author | Lee, Joo Won | - |
dc.date.accessioned | 2021-09-08T16:18:27Z | - |
dc.date.available | 2021-09-08T16:18:27Z | - |
dc.date.created | 2021-06-10 | - |
dc.date.issued | 2009-06 | - |
dc.identifier.issn | 0021-9541 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/119859 | - |
dc.description.abstract | Growing evidence indicates that aldosterone is a potent mitogenic signal regulating genes involved in antiapoptosis, cell proliferation and growth. We investigated the role of endogenous aldosterone in renal development, cell proliferation and apoptosis, and mitogen-activated protein kinase (MAPK) family expression. Newborn rats were treated with either spironolactone (200 mg/kg/d) in olive oil or only olive oil for 7 days. TUNEL assay and proliferating cell nuclear antigen (PCNA) stain were per-formed on kidney sections. Immunoblots, immunohistochemical (IHC) stain, and reverse transcriptase-PCR for MAPKs were performed. PCNA-positive proliferating cells decreased and apoptotic cells increased significantly with spironolactone (P < 0.05). In the spironolactone-treated group, c-jun N-terminal kinase (JNK)-2 expression increased, whereas extracellular signal regulated kinase (ERK)-2 and p38 expressions decreased in immunoblots (P < 0.05) and IHC stain. ERK-2 and p38 mRNA expressions increased in the spironolactone-treated group (P < 0.05). This study demonstrates that aldosterone blockade in the developing kidney decreases cellular proliferation, increases apoptosis, and modulates the expressions of JNK-2, ERK-2, and p38. Aldosterone possibly participates in renal development and MAPK family may serve as, in part, the signaling intermediate through the mineralocorticoid receptor (MR) in the developing kidney. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | WILEY | - |
dc.subject | MAP-KINASES | - |
dc.subject | ERK | - |
dc.subject | PROLIFERATION | - |
dc.subject | HYPERTONICITY | - |
dc.subject | APOPTOSIS | - |
dc.subject | DEATH | - |
dc.subject | CELLS | - |
dc.title | Aldosterone Regulates Cellular Turnover and Mitogen-Activated Protein Kinase Family Expression in the Neonatal Rat Kidney | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Yoo, Kee Hwan | - |
dc.contributor.affiliatedAuthor | Jang, Gi Young | - |
dc.identifier.doi | 10.1002/jcp.21723 | - |
dc.identifier.scopusid | 2-s2.0-64549089670 | - |
dc.identifier.wosid | 000265547900025 | - |
dc.identifier.bibliographicCitation | JOURNAL OF CELLULAR PHYSIOLOGY, v.219, no.3, pp.724 - 733 | - |
dc.relation.isPartOf | JOURNAL OF CELLULAR PHYSIOLOGY | - |
dc.citation.title | JOURNAL OF CELLULAR PHYSIOLOGY | - |
dc.citation.volume | 219 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 724 | - |
dc.citation.endPage | 733 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalResearchArea | Physiology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Physiology | - |
dc.subject.keywordPlus | MAP-KINASES | - |
dc.subject.keywordPlus | ERK | - |
dc.subject.keywordPlus | PROLIFERATION | - |
dc.subject.keywordPlus | HYPERTONICITY | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | DEATH | - |
dc.subject.keywordPlus | CELLS | - |
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