کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
8473435 1550388 2018 46 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Intermittent hypoxia-generated ROS contributes to intracellular zinc regulation that limits ischemia/reperfusion injury in adult rat cardiomyocyte
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
پیش نمایش صفحه اول مقاله
Intermittent hypoxia-generated ROS contributes to intracellular zinc regulation that limits ischemia/reperfusion injury in adult rat cardiomyocyte
چکیده انگلیسی
Intermittent hypoxia (IH) has been shown to exert cardioprotective effects against ischemia/reperfusion (I/R) injury through the preservation of ion homeostasis. I/R dramatically elevated cytosolic Zn2+ and caused cardiomyocyte death. However, the role of IH exposure in the relationship between Zn2+ regulation and cardioprotection is still unclear. The aim of the present study was to study whether IH exposure could help in intracellular Zn2+ regulation, hence contributing to cardioprotection against I/R injury. Adult rat cardiomyocytes were exposed to IH (5% O2, 5% CO2 and balanced N2) for 30 min followed by 30 min of normoxia (21% O2, 5% CO2 and balanced N2). Changes in intracellular Zn2+ concentration were determined using a Zn2+-specific fluorescent dye, FluoZin-3 or RhodZin-3. Fluorescence was monitored under an inverted fluorescent or confocal microscope. The results demonstrated that I/R or 2,2′-dithiodipyridine (DTDP), a reactive disulphide compound, induced Zn2+ release from metallothioneins (MTs), subsequently causing cytosolic Zn2+ overload, which in turn increased intracellular Zn2+ entry into the mitochondria via a Ca2+ uniporter, hence inducing mitochondrial membrane potential loss, and eventually led to cell death. However, the cytosolic Zn2+ overload and cell death caused by I/R or DTDP was significantly reduced by treatment of cardiomyocytes with IH. The findings from this study suggest that IH might exert its cardioprotective effect through reducing the I/R-induced cytosolic Zn2+ overload and cell death in cardiomyocytes.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 118, May 2018, Pages 122-132
نویسندگان
, , , , , ,