کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8475089 | 1550443 | 2013 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Regulation of cardiac nitric oxide signaling by nuclear β-adrenergic and endothelin receptors
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کلمات کلیدی
nuclear factor kappa-light-chain-enhancer of activated B-cellsdiaminofluorescein-2ET-1GPCRCyPEEDQDTTendothelin type B receptorcGMPETRNOSDAF-2βARETBDNA - DNA یا اسید دزوکسی ریبونوکلئیکN-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline - N-ethoxycarbonyl-2-ethoxy-1،2-dihydroquinolineNFκB - NFKBAdenosine Triphosphate - آدنوزین تری فسفاتATP - آدنوزین تری فسفات یا ATPadenylyl cyclase - آدنیلات سیکلاز، آدنیلیل سیکلازdeoxyribonucleic acid - اسید deoxyribonucleicendothelin 1 - اندوتلین 1ISO - ایزوisoproterenol - ایزوپروترنولdithiothreitol - دیتیوتریتولcyanopindolol - سایانوپندولولNitric oxide - نیتریک اکسیدnitric oxide synthase - نیتریک اکسید سنتازcyclic guanosine 3′,5′-monophosphate - گوانوزین سیکل 3 '، 5'-مونوفسفرهguanylyl cyclase - گویینیل سیکلاسα-adrenergic receptor - گیرنده α-adrenergicβ-Adrenergic receptor - گیرنده β-adrenergicEndothelin receptor - گیرنده اندوتلینG protein-coupled receptor - گیرندههای جفتشونده با پروتئین جی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
At the cell surface, βARs and endothelin receptors can regulate nitric oxide (NO) production. β-adrenergic receptors (βARs) and type B endothelin receptors (ETB) are present in cardiac nuclear membranes and regulate transcription. The present study investigated the role of the NO pathway in the regulation of gene transcription by these nuclear G protein-coupled receptors. Nitric oxide production and transcription initiation were measured in nuclei isolated from the adult rat heart. The cell-permeable fluorescent dye 4,5-diaminofluorescein diacetate (DAF2 DA) was used to provide a direct assessment of nitric oxide release. Both isoproterenol and endothelin increased NO production in isolated nuclei. Furthermore, a β3AR-selective agonist, BRL 37344, increased NO synthesis whereas the β1AR-selective agonist xamoterol did not. Isoproterenol increased, whereas ET-1 reduced, de novo transcription. The NO synthase inhibitor l-NAME prevented isoproterenol from increasing either NO production or de novo transcription. l-NAME also blocked ET-1-induced NO-production but did not alter the suppression of transcription initiation by ET-1. Inhibition of the cGMP-dependent protein kinase (PKG) using KT5823 also blocked the ability of isoproterenol to increase transcription initiation. Furthermore, immunoblotting revealed eNOS, but not nNOS, in isolated nuclei. Finally, caged, cell-permeable isoproterenol and endothelin-1 analogs were used to selectively activate intracellular β-adrenergic and endothelin receptors in intact adult cardiomyocytes. Intracellular release of caged ET-1 or isoproterenol analogs increased NO production in intact adult cardiomyocytes. Hence, activation of the NO synthase/guanylyl cyclase/PKG pathway is necessary for nuclear β3ARs to increase de novo transcription. Furthermore, we have demonstrated the potential utility of caged receptor ligands in selectively modulating signaling via endogenous intracellular G protein-coupled receptors.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 62, September 2013, Pages 58-68
Journal: Journal of Molecular and Cellular Cardiology - Volume 62, September 2013, Pages 58-68
نویسندگان
George Vaniotis, Irina Glazkova, Clémence Merlen, Carter Smith, Louis R. Villeneuve, David Chatenet, Michel Therien, Alain Fournier, Artavazd Tadevosyan, Phan Trieu, Stanley Nattel, Terence E. Hébert, Bruce G. Allen,