ArticleThe Journal of pharmacology and experimental therapeutics2009
Essential role of the 90-kilodalton heat shock protein in mediating nongenomic estrogen signaling in coronary artery smooth muscle.
Article in The Journal of pharmacology and experimental therapeutics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- Involvement of NEK2 and NEK9 in LPS - induced endothelial barrier dysfunction.Microvascular research · 2024Article
- Heat shock protein 90 modulates cutaneous vasodilation during an exercise-heat stress, but not during passive whole-body heating in young women.Physiological reports · 2020Article
- Estrogen-related mechanisms in sex differences of hypertension and target organ damage.Biology of sex differences · 2020Review
- G Protein-Coupled Estrogen Receptor 1 Inhibits Angiotensin II-Induced Cardiomyocyte Hypertrophy via the Regulation of PI3K-Akt-mTOR Signalling and Autophagy.International journal of biological sciences · 2019Article
- Article
- The Expanding Complexity of Estrogen Receptor Signaling in the Cardiovascular System.Circulation research · 2016Review
- Estradiol regulates human QT-interval: acceleration of cardiac repolarization by enhanced KCNH2 membrane trafficking.European heart journal · 2016Article
- Ovine HSP90AA1 gene promoter: functional study and epigenetic modifications.Cell stress & chaperones · 2015Article
- β3-Adrenoceptor activation relieves oxidative inhibition of the cardiac Na+-K+ pump in hyperglycemia induced by insulin receptor blockade.American journal of physiology. Cell physiology · 2015Article
- G-protein-coupled estrogen receptor as a new therapeutic target for treating coronary artery disease.World journal of cardiology · 2014Review
- HDAC6 regulates glucocorticoid receptor signaling in serotonin pathways with critical impact on stress resilience.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Modulation of heme/substrate binding cleft of neuronal nitric-oxide synthase (nNOS) regulates binding of Hsp90 and Hsp70 proteins and nNOS ubiquitination.The Journal of biological chemistry · 2012Article
- Testosterone-induced relaxation of coronary arteries: activation of BKCa channels via the cGMP-dependent protein kinase.American journal of physiology. Heart and circulatory physiology · 2012Article
- A cross-species analysis method to analyze animal models' similarity to human's disease state.BMC systems biology · 2012Article
- Activation of G protein-coupled estrogen receptor induces endothelium-independent relaxation of coronary artery smooth muscle.American journal of physiology. Endocrinology and metabolism · 2011Article
- Modulation of α(2C) adrenergic receptor temperature-sensitive trafficking by HSP90.Biochimica et biophysica acta · 2011Article
- The G protein-coupled estrogen receptor GPER/GPR30 as a regulator of cardiovascular function.Vascular pharmacologyReview
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Under normal physiological conditions, estrogen is a coronary vasodilator, and this response involves production of NO from endothelial cells. In addition, estrogen also stimulates NO production in coronary artery smooth muscle (CASM); however, the molecular basis for this nongenomic effect of estrogen is unclear. The purpose of this study was to investigate a potential role for the 90-kDa heat shock protein (Hsp90) in estrogen-stimulated neuronal nitric-oxide synthase (nNOS) activity in coronary artery smooth muscle. 17Beta-estradiol produced a concentration-dependent relaxation of endothelium-denuded porcine coronary arteries in vitro, and this response was attenuated by inhibiting Hsp90 function with 1 microM geldanamycin (GA) or 100 microg/ml radicicol (RAD). These inhibitors also prevented estrogen-stimulated NO production in human CASM cells and reversed the stimulatory effect of estrogen on calcium-activated potassium (BK(Ca)) channels. These functional studies indicated a role for Hsp90 in coupling estrogen receptor activation to NOS stimulation in CASM. Furthermore, coimmunoprecipitation studies demonstrated that estrogen stimulates bimolecular interaction of immunoprecipitated nNOS with Hsp90 and that either GA or RAD could inhibit this association. Blocking estrogen receptors with ICI182780 (fulvestrant) also prevented this association. These findings indicate an essential role for Hsp90 in nongenomic estrogen signaling in CASM and further suggest that Hsp90 might represent a prospective therapeutic target to enhance estrogen-stimulated cardiovascular protection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.