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Cited by 358

The DOI matches its Crossref record; 54 of the 54 references it cites were found in a registry or an index.

Angiotensin II and Aldosterone Regulate Gene Transcription Via Functional Mineralocortocoid Receptors in Human Coronary Artery Smooth Muscle Cells

Open access
Jaffe, Iris Z., Mendelsohn, Michael E.·2005·Circulation Research
DOI 10.1161/01.res.0000159937.05502.d1
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Abstract

Inhibition or blockade of the angiotensin-aldosterone system consistently decreases ischemic cardiovascular events in clinical trials. The steroid hormone aldosterone acts by binding to the mineralocorticoid receptor (MR), a ligand activated transcription factor that is a member of the nuclear hormone receptor superfamily. MR binds and is activated by aldosterone and cortisol with equal affinity, but MR activation by cortisol is diminished in tissues that express the cortisol-inactivating enzyme 11-β-hydroxysteroid-dehydrogenase-2 (11βHSD2). Although previous studies support that the vasculature is a target tissue of aldosterone, MR-mediated gene expression in vascular cells has not been demonstrated or systematically explored. We investigated whether functional MR and 11βHSD2 are expressed in human blood vessels. Human coronary and aortic vascular smooth muscle cells (VSMCs) express mRNA and protein for both MR and 11βHSD2. The endogenous VSMC MR mediates aldosterone-dependent gene expression, which is blocked by the competitive MR antagonist spironolactone. Inhibition of 11βHSD2 in coronary artery VSMCs enhances gene transactivation by cortisol, supporting that the VSMC 11βHSD2 is functional. Angiotensin II also activates MR-mediated gene transcription in coronary artery VSMCs. Angiotensin II activation of MR-mediated gene expression is inhibited by both the AT1 receptor blocker losartan and by spironolactone, but not by aldosterone synthase inhibition. Microarray and quantitative RT-PCR experiments show that aldosterone activates expression of endogenous human coronary VSMC genes, including several involved in vascular fibrosis, inflammation, and calcification. These data support a new MR-dependent mechanism by which aldosterone and angiotensin II influence ischemic cardiovascular events, and suggest that ACE inhibitors and MR antagonists may decrease clinical ischemic events by inhibiting MR-dependent gene expression in vascular cells.

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Metadata

Authors
Jaffe, I. Z., & Mendelsohn, M. E.
Venue
Circulation Research
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2005-04
Volume
96
Issue
6
Pages
643-650
ISSN
  • 0009-7330 (ISSN-L)
  • 1524-4571
DOI
10.1161/01.res.0000159937.05502.d1
OpenAlex
W2010743737
Cited by
358
References
54
FWCI
9.85
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Angiotensin II and Aldosterone Regulate Gene Transcription Via Functional Mineralocortocoid Receptors in Human Coronary Artery Smooth Muscle Cells. https://app.cochat.ai/papers/10.1161/01.res.0000159937.05502.d1
The paper
Jaffe, I. Z., & Mendelsohn, M. E. (2005). Angiotensin II and Aldosterone Regulate Gene Transcription Via Functional Mineralocortocoid Receptors in Human Coronary Artery Smooth Muscle Cells. Circulation Research. https://doi.org/10.1161/01.res.0000159937.05502.d1

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.