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- W1968016736 abstract "We previously showed that aldosterone augmented angiotensin converting enzyme (ACE) gene expression in cultured rat cardiac fibroblasts (CF). Here, we tested hypothesis that aldosterone exhibit the above effect thorugh glucocorticoid receptor (GR), because the same effect as aldosterone was observed in case with cortisol even in lower dosage. CF were prepared from neonatal rat, and ACE gene expression was quantified by real-time RT-PCR. Gene and protein expression of GR, mineralocorticoid receptor (MR), and 11beta-hydroxysterod dehydrogenase (11b-HSD) were examined from cardiocytes and tissue homogenate. In heart homogenate, expression of MR and GR were comparable to kidney and liver, respectively. In CF, however, little amount of MR was expressed, while GR expression was abundant especially in cytoplasm. 11b-HSD type1 was expressed abundantly, on the other hand, 11b-HSD type2 was not expressed in CF. These findings strongly supported the possibility that aldosterone failed to bind MR in CF. We found that not RU28313 (a specific MR antagonist) but mifepristone (a specific GR antagonist) antagonized effects of aldosterone. Moreover, knock-down of GR by siRNA but not MR, which resulted in the gene expression levels reduced to ∼30%, abolished augmentation of ACE gene expression by aldosterone. These findings indicate that aldosterone augments ACE gene expression through GR in CF, and blockade of GR may be novel therapeutic target of chronic heart failure." @default.
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- W1968016736 date "2005-12-01" @default.
- W1968016736 modified "2023-10-18" @default.
- W1968016736 title "Glucocorticoid Receptor is Requisite for Aldosterone-Augmented Angiotensin Converting Enzyme Gene Expression in Cardiac Fibroblasts" @default.
- W1968016736 doi "https://doi.org/10.1016/j.cardfail.2005.08.320" @default.
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