کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10953841 | 1097813 | 2012 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Epac enhances excitation-transcription coupling in cardiac myocytes
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کلمات کلیدی
NCXET-1PLCRyRPBSIP3R2-APB2-aminoethoxydiphenyl borateEpacPKCband passHdac5GEFn.a.Ca2 +-induced Ca2 + releasesarco/endoplasmic reticulum Ca2 +-ATPaseinositol 1,4,5 triphosphateIP3pKaCaMKIISDSMEF2GFPDAPIBSA - BSACa2 +/calmodulin-dependent protein kinase II - Ca2 + / calmodulin وابسته پروتئین کیناز II[Ca2 +]i - [Ca2 +] ibovine serum albumin - آلبومین سرم گاوendothelin-1 - اندوتلین-1excitation–contraction - تحریک-انقباضExcitation–contraction coupling - تحریک-انقباض جفت شدنExcitation–transcription coupling - تحریک-رونویسی کوپلینگRoom temperature - دمای اتاقSarcoplasmic reticulum - رتیکولوم سارکوپلاسمیکsodium dodecyl sulphate - سدیم دودسیل سولفاتCalcium signaling - سیگنالینگ کلسیمCalcium concentration - غلظت کلسیمwater immersion - غوطه وری آبmyocyte enhancer factor 2 - فاکتور افزایش دهنده myocyte 2Phosphate buffered saline - فسفات بافر شورphospholipase C - فسفولیپاز CSERCA - قلبVentricular myocyte - میوسیت بطنیHistone deacetylase 5 - هیستون دیازتیلاز 5protein kinase A - پروتئین کیناز AProtein kinase C - پروتئین کیناز سیCICR - کمیته بینالمللی صلیب سرخRyanodine receptor - گیرنده رایانودین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Epac is a guanine nucleotide exchange protein that is directly activated by cAMP, but whose cardiac cellular functions remain unclear. It is important to understand cardiac Epac signaling, because it is activated in parallel to classical cAMP-dependent signaling via protein kinase A. In addition to activating contraction, Ca2Â + is a key cardiac transcription regulator (excitation-transcription coupling). It is unknown how myocyte Ca2Â + signals are decoded in cardiac myocytes to control nuclear transcription. We examine Epac actions on cytosolic ([Ca2Â +]i) and intranuclear ([Ca2Â +]n) Ca2Â + homeostasis, focusing on whether Epac alters [Ca2Â +]n and activates a prohypertrophic program in cardiomyocytes. Adult rat cardiomyocytes, loaded with fluo-3 were viewed by confocal microscopy during electrical field stimulation at 1Â Hz. Acute Epac activation by 8-pCPT increased Ca2Â + sparks and diastolic [Ca2Â +]i, but decreased systolic [Ca2Â +]i. The effects on diastolic [Ca2Â +]i and Ca2Â + spark frequency were dependent on phospholipase C (PLC), inositol 1,4,5 triphosphate receptor (IP3R) and CaMKII activation. Interestingly, Epac preferentially increased [Ca2Â +]n during both diastole and systole, correlating with the perinuclear expression pattern of Epac. Moreover, Epac activation induced histone deacetylase 5 (HDAC5) nuclear export, with consequent activation of the prohypertrophic transcription factor MEF2. These data provide the first evidence that the cAMP-binding protein Epac modulates cardiac nuclear Ca2Â + signaling by increasing [Ca2Â +]n through PLC, IP3R and CaMKII activation, and initiates a prohypertrophic program via HDAC5 nuclear export and subsequent activation of the transcription factor MEF2.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 52, Issue 1, January 2012, Pages 283-291
Journal: Journal of Molecular and Cellular Cardiology - Volume 52, Issue 1, January 2012, Pages 283-291
نویسندگان
Laetitia Pereira, Gema Ruiz-Hurtado, Eric Morel, Anne-Coline Laurent, Mélanie Métrich, Alejandro DomÃnguez-RodrÃguez, Sandra Lauton-Santos, Alexandre Lucas, Jean-Pierre Benitah, Donald M. Bers, Frank Lezoualc'h, Ana M. Gómez,