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| Reference : Acute cardiovascular protective effects of corticosteroids are mediated by non-transcrip... |
| Scientific journals : Article | |||
| Life sciences : Biochemistry, biophysics & molecular biology Life sciences : Anatomy (cytology, histology, embryology...) & physiology | |||
| http://hdl.handle.net/2268/12174 | |||
| Acute cardiovascular protective effects of corticosteroids are mediated by non-transcriptional activation of endothelial nitric oxide synthase. | |
| English | |
| Hafezi-Moghadam, Ali [Harvard Medical School > Pathology > > >] | |
| Simoncini, Tommaso [University of Pïsa > Reproductive Medicine and Child Development > > >] | |
| Yang, Zequan [University of Vriginia > Biomedial Engineering > > >] | |
| Limbourg, Florian P [Brigham & Women's Hospital and Harveard Medical School > Medicine > > >] | |
Plumier, Jean-Christophe  [Université de Liège - ULg > Département des sciences et gestion de l'environnement > Ecophysiologie et physiologie animale >] | |
| Rebsamen, Michael C [Brigham & Women's Hospital and Harvard Medical School > Medicine > > >] | |
| Hsieh, Chung-Ming [Brigham & Women's Hospital and Harvard Medical School > Medicine > > >] | |
| Chui, Dao-Shan [Brigham & Women's Hospital and Harvard Medical School > Medicine > > >] | |
| Thomas, Kennard L [Harvard Medical School and University of Virginia > > > >] | |
| Prorock, Alyson J [University of Virginia > Biomedical Engineering > > >] | |
| Laubach, Victor E [University of Virginia > Surgery > > >] | |
| Moskowitz, Michael A [Massachusetts General Hospital and Harvard Medical School > > > >] | |
| French, Brent A [University of Virginia > Biomedical Engineering > > >] | |
| Ley, Klaus [University of Virginia > Biomedical Engineering > > >] | |
| Liao, James K [Brigham & Women's Hospital and Harvard Medical School > Medicine > Vascula Medicine > >] | |
| 2002 | |
| Nature Medicine | |
| Nature Publishing Group | |
| 8 | |
| 5 | |
| 473-9 | |
| International | |
| 1078-8956 | |
| 1546-170X | |
| New York | |
| NY | |
| [en] Adrenal Cortex Hormones/pharmacology ; Animals ; Aorta/drug effects/physiology ; Cardiotonic Agents/pharmacology ; Cells, Cultured ; Dexamethasone/pharmacology ; Endothelium, Vascular/enzymology/physiology ; Enzyme Activation/drug effects ; Humans ; Mice ; Muscle Contraction/drug effects/physiology ; Muscle, Smooth, Vascular/physiology ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitric Oxide Synthase/metabolism ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase Type III ; Potassium Chloride | |
| [en] Corticosteroids have been shown to exert beneficial effects in the treatment of acute myocardial infarction, but the precise mechanisms underlying their protective effects are unknown. Here we show that high-dose corticosteroids exert cardiovascular protection through a novel mechanism involving the rapid, non-transcriptional activation of endothelial nitric oxide synthase (eNOS). Binding of corticosteroids to the glucocorticoid receptor (GR) stimulated phosphatidylinositol 3-kinase and protein kinase Akt, leading to eNOS activation and nitric oxide dependent vasorelaxation. Acute administration of pharmacological concentrations of corticosteroids in mice led to decreased vascular inflammation and reduced myocardial infarct size following ischemia and reperfusion injury. These beneficial effects of corticosteroids were abolished by GR antagonists or eNOS inhibitors in wild-type mice and were completely absent in eNOS-deficient (Nos3(-/-)) mice. The rapid activation of eNOS by the non-nuclear actions of GR, therefore, represents an important cardiovascular protective effect of acute high-dose corticosteroid therapy. | |
| http://hdl.handle.net/2268/12174 | |
| 10.1038/nm0502-473 |
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