کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
10802928 1055735 2010 11 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Infection with AV-SUR2A protects H9C2 cells against metabolic stress: A mechanism of SUR2A-mediated cytoprotection independent from the KATP channel activity
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Infection with AV-SUR2A protects H9C2 cells against metabolic stress: A mechanism of SUR2A-mediated cytoprotection independent from the KATP channel activity
چکیده انگلیسی
Transgenic mice overexpressing SUR2A, a subunit of ATP-sensitive K+ (KATP) channels, acquire resistance to myocardial ischaemia. However, the mechanism of SUR2A-mediated cytoprotection is yet to be fully understood. Adenoviral SUR2A construct (AV-SUR2A) increased SUR2A expression, number of KATP channels and subsarcolemmal ATP in glycolysis-sensitive manner in H9C2 cells. It also increased K+ current in response to chemical hypoxia, partially preserved subsarcolemmal ATP and increased cell survival. Kir6.2AFA, a mutant form of Kir6.2 with largely decreased K+ conductance, abolished the effect of SUR2A on K+ current, did not affect SUR2A-induced increase in subsarcolemmal ATP and partially inhibited SUR2A-mediated cytoprotection. Infection with 193gly-M-LDH, an inactive mutant of muscle lactate dehydrogenase, abolished the effect of SUR2A on K+ current, subsarcolemmal ATP and cell survival; the effect of 193gly-M-LDH on cell survival was significantly more pronounced than those of Kir6.2AFA. We conclude that AV-SUR2A increases resistance to metabolic stress in H9C2 cells by increasing the number of sarcolemmal KATP channels and subsarcolemmal ATP.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1803, Issue 3, March 2010, Pages 405-415
نویسندگان
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