کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10835168 | 1066044 | 2011 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Nitric oxide regulates pulmonary vascular smooth muscle cell expression of the inducible cAMP early repressor gene
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کلمات کلیدی
VASPPKGAT2RSGCVSMCCREBICERTGF-β3MT1NOS2m.o.i.metallothionein 1heme-oxygenase 1VDCCHK2Et1HO1kinase-inducible domainp-CREBCREβgaltPAPDESOCCIL-1βcyclic GMP - GMP دوره ایAdenovirus - آدنوویروسendothelin 1 - اندوتلین 1Interleukin-1β - اینترلوکین-1βbeta-galactosidase - بتا گالاکتوزیدازKid - بچهTransforming growth factor-β3 - تبدیل فاکتور رشد β3Inducible cAMP early repressor - سرکوب کننده اولیه cAMP قابل انعطاف استVascular smooth muscle cells - سلول های عضلانی صاف عروقیSoluble guanylate cyclase - سیکلاس گوانیلات حل کنندهVascular smooth muscle - عضله صاف عضلانیcAMP-response element - عنصر پاسخ cAMPphosphorylated CREB - فرسورده CREBPhosphodiesterase - فسفو دی استرازVasodilator-stimulated phosphoprotein - فسفوپروتئین تحریک شده با واسوادولاتورtissue plasminogen activator - فعال کننده بافتی پلاسمینوژنNitric oxide - نیتریک اکسیدnitric oxide synthase 2 - نیتریک اکسید سنتاز 2CRE-binding protein - پروتئین CRE-bindingprotein kinase A - پروتئین کیناز AcGMP-dependent protein kinase - پروتئین کیناز وابسته به cGMPmultiplicity of infection - چندین عفونتVoltage-dependent calcium channels - کانال های کلسیم وابسته به ولتاژCREm - کرم رنگAngiotensin II receptor - گیرنده آنژیوتانسین II
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Nitric oxide (NO) regulates vascular smooth muscle cell (VSMC) structure and function, in part by activating soluble guanylate cyclase (sGC) to synthesize cGMP. The objective of this study was to further characterize the signaling mechanisms by which NO regulates VSMC gene expression using transcription profiling. DNA microarrays were hybridized with RNA extracted from rat pulmonary artery smooth muscle cells (RPaSMC) exposed to the NO donor compound, S-nitroso-glutathione (GSNO). Many of the genes, whose expression was induced by GSNO, contain a cAMP-response element (CRE), of which one encoded the inducible cAMP early repressor (ICER). sGC and cAMP-dependent protein kinase, but not cGMP-dependent protein kinase, were required for NO-mediated phosphorylation of CRE-binding protein (CREB) and induction of ICER gene expression. Expression of a dominant-negative CREB in RPaSMC prevented the NO-mediated induction of CRE-dependent gene transcription and ICER gene expression. Pre-treatment of RPaSMC with the intracellular calcium (Ca2+) chelator, BAPTA-AM, blocked the induction of ICER gene expression by GSNO. The store-operated Ca2+ channel inhibitors, 2-ABP, and SKF-96365, reduced the GSNO-mediated increase in ICER mRNA levels, while 2-ABP did not inhibit GSNO-induced CREB phosphorylation. Our results suggest that induction of ICER gene expression by NO requires both CREB phosphorylation and Ca2+ signaling. Transcription profiling of RPaSMC exposed to GSNO revealed important roles for sGC, PKA, CREB, and Ca2+ in the regulation of gene expression by NO. The induction of ICER in GSNO-treated RPaSMC highlights a novel cross-talk mechanism between cGMP and cAMP signaling pathways.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Nitric Oxide - Volume 25, Issue 3, 30 October 2011, Pages 294-302
Journal: Nitric Oxide - Volume 25, Issue 3, 30 October 2011, Pages 294-302
نویسندگان
Andrea U. Steinbicker, Heling Liu, Kim Jiramongkolchai, Rajeev Malhotra, Elizabeth Y. Choe, Cornelius J. Busch, Amanda R. Graveline, Sonya M. Kao, Yasuko Nagasaka, Fumito Ichinose, Emmanuel S. Buys, Peter Brouckaert, Warren M. Zapol, Kenneth D. Bloch,