Aldosterone Modulates Cell Proliferation and Apoptosis in the Neonatal Rat Heart.
10.3346/jkms.2010.25.9.1296
- Author:
Hyung Joo SOHN
1
;
Kee Hwan YOO
;
Gi Young JANG
;
Jang Hoon LEE
;
Byung Min CHOI
;
Jung Hwa LEE
;
In Sun BAE
;
Hyung Eun YIM
;
Chang Sung SON
;
Joo Won LEE
Author Information
1. Department of Pediatrics, Korea University College of Medicine, Korea University Hospital, Seoul, Korea. JGYNHG@yahoo.co.kr
- Publication Type:Original Article
- Keywords:
Aldosterone;
Muscle Cells;
Apoptosis;
Cell Proliferation
- MeSH:
Aldosterone Antagonists/*pharmacology;
Animals;
Animals, Newborn;
*Apoptosis;
Cell Proliferation;
Clusterin/genetics/metabolism;
Female;
Heart/*drug effects/growth & development;
Proliferating Cell Nuclear Antigen/metabolism;
Rats;
Rats, Sprague-Dawley;
Spironolactone/*pharmacology;
Transforming Growth Factor beta2/genetics/metabolism;
Tumor Suppressor Protein p53/genetics/metabolism;
p38 Mitogen-Activated Protein Kinases/genetics/metabolism
- From:Journal of Korean Medical Science
2010;25(9):1296-1304
- CountryRepublic of Korea
- Language:English
-
Abstract:
In the present study, we investigated whether and how the mineralocorticoid receptor antagonist spironolactone affects cardiac growth and development through apoptosis and cell proliferation in the neonatal rat heart. Newborn rat pups were treated with spironolactone (200 mg/kg/d) for 7 days. The cell proliferation was studied by PCNA immunostaining. The treatment with spironolactone decreased proliferating myocytes by 32% (P<0.05), and reduced myocytes apoptosis by 29% (P<0.05). Immunoblot and immunohistochemistry for the expression of p38, p53, clusterin, TGF-beta2, and extracellular signal-regulated kinase were performed. In the spironolactone group, p38, p53, clusterin, and TGF-beta2 protein expression was significantly decreased (P<0.05). These results indicate that aldosterone inhibition in the developing rat heart induces cardiac growth impairment by decreasing proliferation and apoptosis of myocytes.
