Aldosterone regulates cellular turnover and mitogen-activated protein kinase family expression in the neonatal rat kidney

Eun Yim Hyung, Hwan Yoo Kee, Sun Bae In, Young Jang Gi, Sook Hong Young, Won Lee Joo

Research output: Contribution to journalArticle

17 Citations (Scopus)

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 performed 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.

Original languageEnglish
Pages (from-to)724-733
Number of pages10
JournalJournal of Cellular Physiology
Volume219
Issue number3
DOIs
Publication statusPublished - 2009 Jun

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

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