کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8474949 | 1550437 | 2014 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Stimulation of NOX2 in isolated hearts reversibly sensitizes RyR2 channels to activation by cytoplasmic calcium
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کلمات کلیدی
RNSO2−·HEDTACa2 +-induced Ca2 + releaseRyRGSHEGTADTTRyR2ROS - ROSsuperoxide anion - آنیون سوپر اکسیدischemia/reperfusion - ایسکمی / رپرفیوژنSingle channel - تک کانالdithiothreitol - دیتیوتریتولSarcoplasmic reticulum - رتیکولوم سارکوپلاسمیکRedox signaling - سیگنالینگ Redoxendoplasmic reticulum - شبکه آندوپلاسمی phosphatidylcholine - فسفاتیدیل کولینPhosphatidylserine - فسفاتیدیلسرینPOPE - پاپPreconditioning - پیش شرط بندیGlutathione - گلوتاتیونreactive nitrogen species - گونه های واکنش پذیر نیتروژنReactive oxygen species - گونههای فعال اکسیژنRyanodine receptor - گیرنده رایانودین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The response of ryanodine receptor (RyR) channels to cytoplasmic free calcium concentration ([Ca2Â +]) is redox sensitive. Here, we report the effects of a mild oxidative stress on cardiac RyR (RyR2) channels in Langendorff perfused rat hearts. Single RyR2 channels from control ventricles displayed the same three responses to Ca2Â + reported in other mammalian tissues, characterized by low, moderate, or high maximal activation. A single episode of 5Â min of global ischemia, followed by 1Â min of reperfusion, enhanced 2.3-fold the activity of NOX2 compared to controls and changed the frequency distribution of the different responses of RyR2 channels to calcium, favoring the more active ones: high activity response increased and low activity response decreased with respect to controls. This change was fully prevented by perfusion with apocynin or VAS 2870 before ischemia and totally reversed by the extension of the reperfusion period to 15Â min. In vitro activation of NOX2 in control SR vesicles mimicked the effect of the ischemia/reperfusion episode on the frequencies of emergence of single RyR2 channel responses to [Ca2Â +] and increased 2.2-fold the rate of calcium release in Ca2Â +-loaded SR vesicles. In vitro changes were reversed at the single channel level by DTT and in isolated SR vesicles by glutaredoxin. Our results indicate that in whole hearts a mild oxidative stress enhances the response of cardiac RyR2 channels to calcium via NOX2 activation, probably by S-glutathionylation of RyR2 protein. This change is transitory and fully reversible, suggesting a possible role of redox modification in the physiological response of cardiac RyR2 to cellular calcium influx.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 68, March 2014, Pages 38-46
Journal: Journal of Molecular and Cellular Cardiology - Volume 68, March 2014, Pages 38-46
نویسندگان
Paulina Donoso, José Pablo Finkelstein, Luis Montecinos, Matilde Said, Gina Sánchez, Leticia Vittone, Ricardo Bull,