کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5507262 | 1400322 | 2017 | 58 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Identity and function of a cardiac mitochondrial small conductance Ca2+-activated K+ channel splice variant
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کلمات کلیدی
COXPPCeGFPmitotracker redCaMBDMCU1-ethyl-2-benzimidazolinoneMPTPΔΨmCyPPAEDHFMTRAPDBSA - BSAbovine serum albumin - آلبومین سرم گاوmitochondrial permeability transition pore - انتقال نفوذی میتوکندری منفی استimm - انحصارischemia/reperfusion - ایسکمی / رپرفیوژنinner mitochondrial membrane - درونی غشای میتوکندریcytochrome c oxidase - سیتوکروم سی اکسیدازLAD - لادوMitochondrial Ca2+ uniporter - متقاطع کلسیم + mitochondrial uniporterAction potential duration - مدت زمان بالقوه عملhypoxia/reoxygenation - هیپوکسیا / اکسیداسیون مجددMitochondrial membrane potential - پتانسیل غشای میتوکندریenhanced green fluorescent protein - پروتئین فلورسنت سبز افزایش یافته استleft anterior descending coronary artery - چپ قدامی نزولی عروق کرونر
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم کشاورزی و بیولوژیک
دانش گیاه شناسی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
We provide evidence for location and function of a small conductance, Ca2+-activated K+ (SKCa) channel isoform 3 (SK3) in mitochondria (m) of guinea pig, rat and human ventricular myocytes. SKCa agonists protected isolated hearts and mitochondria against ischemia/reperfusion (IR) injury; SKCa antagonists worsened IR injury. Intravenous infusion of a SKCa channel agonist/antagonist, respectively, in intact rats was effective in reducing/enhancing regional infarct size induced by coronary artery occlusion. Localization of SK3 in mitochondria was evidenced by Western blot of inner mitochondrial membrane, immunocytochemical staining of cardiomyocytes, and immunogold labeling of isolated mitochondria. We identified a SK3 splice variant in guinea pig (SK3.1, aka SK3a) and human ventricular cells (SK3.2) by amplifying mRNA, and show mitochondrial expression in mouse atrial tumor cells (HL-1) by transfection with full length and truncated SK3.1 protein. We found that the N-terminus is not required for mitochondrial trafficking but the C-terminus beyond the Ca2+ calmodulin binding domain is required for Ca2+ sensing to induce mK+ influx and/or promote mitochondrial localization. In isolated guinea pig mitochondria and in SK3 overexpressed HL-1 cells, mK+ influx was driven by adding CaCl2. Moreover, there was a greater fall in membrane potential (ÎΨm), and enhanced cell death with simulated cell injury after silencing SK3.1 with siRNA. Although SKCa channel opening protects the heart and mitochondria against IR injury, the mechanism for favorable bioenergetics effects resulting from SKCa channel opening remains unclear. SKCa channels could play an essential role in restraining cardiac mitochondria from inducing oxidative stress-induced injury resulting from mCa2+ overload.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Bioenergetics - Volume 1858, Issue 6, June 2017, Pages 442-458
Journal: Biochimica et Biophysica Acta (BBA) - Bioenergetics - Volume 1858, Issue 6, June 2017, Pages 442-458
نویسندگان
MeiYing Yang, Amadou K.S. Camara, Mohammed Aldakkak, Wai-Meng Kwok, David F. Stowe,