Neuronal Ca2+ sensor-1 contributes to stress tolerance in cardiomyocytes via activation of mitochondrial detoxification pathways
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- 作者：Tomoe Y. Nakamuraa ; tomoen@ri.ncvc.go.jp" class="auth_mail" title="E-mail the corresponding author ; tomoe.no1@gmail.com" class="auth_mail" title="E-mail the corresponding author ; Shu Nakaoa ; 1 ; Shigeo Wakabayashia ; b ; 2
- 关键词：Akt ; protein kinase B ; AMPK ; AMP-activated protein kinase ; ATP ; adenosine triphosphate ; CaMKII ; Ca2+/calmodulin-dependent protein kinase II ; FCCP ; carbonyl cyanide-p-trifluoromethoxyphenylhydrazone ; GAPDH ; glyceraldehyde 3-phosphate dehydrogenase ; GSK3β ; glycogen synthase kinase 3 beta ; H2O2 ; hydrogen peroxide ; I/R ; ischemia-reperfusion ; LDH ; lactate dehydrogenase ; NMVM ; neonatal mouse ventricular myocyte ; NCS-1 ; neuronal calcium sensor-1 ; OCR ; oxygen consumption rate ; PGC-1α ; peroxisome prolife
- 刊名：Journal of Molecular and Cellular Cardiology
- 出版年：2016
- 出版时间：October 2016
- 年：2016
- 卷：99
- 期：Complete
- 页码：23-34
- 全文大小：2070 K
文摘
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NCS-1 knockout rendered mouse hearts more susceptible to oxidative/metabolic stress.
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10">Re-expression of NCS-1 partially rescued cardiomyocytes from H2O2-induced toxicity
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15">ATP levels, mitochondrial respiration and protein levels were lower in KO myocytes.
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NCS-1 expression reversed early ΔΨm loss in KO myocytes induced by H2O2.
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Stress-induced cardioprotective pathways were inhibited in KO hearts and myocytes.