Transcriptomics

Dataset Information

3

Effect of Mineralocorticoid Receptor deletion on glucocorticoid signalling in the macropahge


ABSTRACT: Inappropriate excess of the steroid hormone aldosterone, which is a mineralocorticoid receptor (MR) agonist, is associated with increased inflammation and risk of cardiovascular disease. MR antagonists are cardioprotective and antiinflammatory in vivo, and evidence suggests that they mediate these effects in part by aldosterone- independent mechanisms. We used affymetrix to characterize the effect of Mineralocorticoid Receptor deletion on macrophage transcriptional profile, and identify its requirement in normal glucocorticoid signalling. We isolated mouse peritoneal macrophages from Myeloid MRKO mice and Floxed Controls, cultured in the presence or absence of corticosterone. RNA was extracted for Affymetrix cDNA hybridization. Each sample was pooled from experiments performed in triplicate.

ORGANISM(S): Mus musculus  

SUBMITTER: Sheng Z Duan   Carey Lumeng  Ryan A Frieler  Richard M Mortensen  Christine Ivaschenko  Stefan Berger  Gunther Schutz  mort lab  Michael Usher 

PROVIDER: E-GEOD-23308 | ArrayExpress | 2010-07-30

SECONDARY ACCESSION(S): GSE23308PRJNA131199

REPOSITORIES: GEO, ArrayExpress

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Publications

Myeloid mineralocorticoid receptor controls macrophage polarization and cardiovascular hypertrophy and remodeling in mice.

Usher Michael G MG   Duan Sheng Zhong SZ   Ivaschenko Christine Y CY   Frieler Ryan A RA   Berger Stefan S   Schütz Günther G   Lumeng Carey N CN   Mortensen Richard M RM  

The Journal of clinical investigation 20100809 9


Inappropriate excess of the steroid hormone aldosterone, which is a mineralocorticoid receptor (MR) agonist, is associated with increased inflammation and risk of cardiovascular disease. MR antagonists are cardioprotective and antiinflammatory in vivo, and evidence suggests that they mediate these effects in part by aldosterone-independent mechanisms. Here we have shown that MR on myeloid cells is necessary for efficient classical macrophage activation by proinflammatory cytokines. Macrophages f  ...[more]

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