Journal Article

Activation of the Mineralocorticoid Receptor Increases Striatin Levels

Luminita H. Pojoga, Patricia Coutinho, Alicia Rivera, Tham M. Yao, Enrique R. Maldonado, Rodeler Youte, Gail K. Adler, Jonathan Williams, Alexander Turchin, Gordon H. Williams and Jose R. Romero

in American Journal of Hypertension

Published on behalf of American Journal of Hypertension, Ltd.

Volume 25, issue 2, pages 243-249
Published in print February 2012 | ISSN: 0895-7061
Published online February 2012 | e-ISSN: 1941-7225 | DOI: https://dx.doi.org/10.1038/ajh.2011.197
Activation of the Mineralocorticoid Receptor Increases Striatin Levels

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Show all results sharing these subjects:

  • Neuroendocrinology and Autonomic Nervous System
  • Biochemistry
  • Endocrinology and Diabetes

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Background:

Aldosterone (ALDO), a critical regulator of sodium homeostasis, mediates its effects via activation of the mineralocorticoid receptor (MR) through mechanisms that are not entirely clear. Striatin, a membrane associated protein, interacts with estrogen receptors in endothelial cells.

Methods

We studied the effects of MR activation in vitro and in vivo on striatin levels in vascular tissue.

Results

We observed that dietary sodium restriction was associated with increased striatin levels in mouse heart and aorta and that striatin and MR are present in the human endothelial cell line, (EA.hy926), and in mouse aortic endothelial cells (MAEC). Further, we show that MR co-precipitates with striatin in vascular tissue. Incubation of EA.hy926 cells with ALDO (10−8 mol/l for 5–24 h) increases striatin protein and mRNA expression, an effect that was inhibited by canrenoic acid, an MR antagonist. Consistent with these observations, incubation of MAEC with ALDO increased striatin levels that were likewise blocked by canrenoic acid. To test the in vivo relevance of these findings, we studied two previously described mouse models of increased ALDO levels. Intraperitoneal ALDO administration augmented the abundance of striatin protein in mouse heart. We also observed that in a murine model of chronic ALDO-mediated cardiovascular damage following treatment with NG-nitro-L-arginine methyl ester plus angiotensin II an increased abundance of striatin protein in heart and kidney tissue.

Conclusion

Our results provide evidence that increased striatin levels is a component of MR activation in the vasculature and suggest that regulation of striatin by ALDO may modulate estrogen’s nongenomic effects.

Keywords: aldosterone; angiotensin; animal physiology; antagonists; blood pressure; endothelial cells; heart tissue; hypertension; inflammation; L-NAME; mineralocorticoid receptor; RAAS

Journal Article.  5033 words.  Illustrated.

Subjects: Neuroendocrinology and Autonomic Nervous System ; Biochemistry ; Endocrinology and Diabetes

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