Journal
HYPERTENSION
Volume 59, Issue 5, Pages 966-+Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/HYPERTENSIONAHA.111.187872
Keywords
transgenic mice; cardiomyocyte; cardiac cell lines; chromatin immunoprecipitation; mineralocorticoid receptor
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Funding
- Ministere de la Recherche
- Region Ile-de-France (CODDIM)
- Institut National de la Sante et de la Recherche Medicate (CoPoc)
- Agence Nationale pour la Recherche [ANR-09-BLAN-0156-01, ANR-09-EBIO-024-01]
- Programme National de Recherche Cardiovasculaire
- Institut National de la Sante et de la Recherche Medicale
- Societe Francaise d'Hypertension arterielle
- Ministerio de Ciencia e Innovacion (Spain) [BFU2010-16265]
- Consolider [SICI-CSD2008-000005]
- Agence Nationale de la Recherche (ANR) [ANR-09-BLAN-0156] Funding Source: Agence Nationale de la Recherche (ANR)
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Mineralocorticoid receptor (MR) activation may be deleterious to the cardiovascular system, and MR antagonists improve morbidity and mortality of patients with heart failure. However, mineralocorticoid signaling in the heart remains largely unknown. Using a pan-genomic transcriptomic analysis, we identified neutrophil gelatinase-associated lipocalin (NGAL or lipocalin 2) as a strongly induced gene in the heart of mice with conditional and targeted MR overexpression in cardiomyocytes (whereas induction was low in glucocorticoid receptor-overexpressing mice). NGAL mRNA levels were enhanced after hormonal stimulation by the MR ligand aldosterone in cultured cardiac cells and in the heart of wild-type mice. Mineralocorticoid pathological challenge induced by nephrectomy/aldosterone/salt treatment upregulated NGAL expression in the heart and aorta and its plasma levels. We show evidence for MR binding to an NGAL promoter, providing a mechanism for NGAL regulation. We propose that NGAL may be a marker of mineralocorticoid-dependent injury in the cardiovascular system in mice. (Hypertension. 2012;59:966-972.) . Online Data Supplement
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