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Ca+2Calmodulin-Dependent Protein Kinase Mediates Glucose Toxicity-Induced Cardiomyocyte Contractile Dysfunction
المؤلفون المشاركون
Zhang, Rong-Huai
Kandadi, Machender R.
Guo, Haitao
Ren, Jun
Wang, Xiao-Ming
المصدر
العدد
المجلد 2012، العدد 2012 (31 ديسمبر/كانون الأول 2011)، ص ص. 1-11، 11ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2012-04-10
دولة النشر
مصر
عدد الصفحات
11
التخصصات الرئيسية
الملخص EN
(1) Hyperglycemia leads to cytotoxicity in the heart.
Although several theories are postulated for glucose toxicity-induced cardiomyocyte dysfunction, the precise mechanism still remains unclear.
(2) This study was designed to evaluate the impact of elevated extracellular Ca2+ on glucose toxicity-induced cardiac contractile and intracellular Ca2+ anomalies as well as the mechanism(s) involved with a focus on Ca2+/calmodulin (CaM)-dependent kinase.
Isolated adult rat cardiomyocytes were maintained in normal (NG, 5.5 mM) or high glucose (HG, 25.5 mM) media for 6-12 hours.
Contractile indices were measured including peak shortening (PS), maximal velocity of shortening/relengthening (±dL/dt), time-to-PS (TPS), and time-to-90% relengthening (TR90).
(3) Cardiomyocytes maintained with HG displayed abnormal mechanical function including reduced PS, ±dL/dt, and prolonged TPS, TR90 and intracellular Ca2+ clearance.
Expression of intracellular Ca2+ regulatory proteins including SERCA2a, phospholamban and Na+-Ca2+ exchanger were unaffected whereas SERCA activity was inhibited by HG.
Interestingly, the HG-induced mechanical anomalies were abolished by elevated extracellular Ca2+ (from 1.0 to 2.7 mM).
Interestingly, the high extracellular Ca2+-induced beneficial effect against HG was abolished by the CaM kinase inhibitor KN93.
(4) These data suggest that elevated extracellular Ca2+ protects against glucose toxicity-induced cardiomyocyte contractile defects through a mechanism associated with CaM kinase.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Zhang, Rong-Huai& Guo, Haitao& Kandadi, Machender R.& Wang, Xiao-Ming& Ren, Jun. 2012. Ca+2Calmodulin-Dependent Protein Kinase Mediates Glucose Toxicity-Induced Cardiomyocyte Contractile Dysfunction. Journal of Diabetes Research،Vol. 2012, no. 2012, pp.1-11.
https://search.emarefa.net/detail/BIM-994096
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Zhang, Rong-Huai…[et al.]. Ca+2Calmodulin-Dependent Protein Kinase Mediates Glucose Toxicity-Induced Cardiomyocyte Contractile Dysfunction. Journal of Diabetes Research Vol. 2012, no. 2012 (2011), pp.1-11.
https://search.emarefa.net/detail/BIM-994096
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Zhang, Rong-Huai& Guo, Haitao& Kandadi, Machender R.& Wang, Xiao-Ming& Ren, Jun. Ca+2Calmodulin-Dependent Protein Kinase Mediates Glucose Toxicity-Induced Cardiomyocyte Contractile Dysfunction. Journal of Diabetes Research. 2012. Vol. 2012, no. 2012, pp.1-11.
https://search.emarefa.net/detail/BIM-994096
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-994096
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