Roles of Endoplasmic Reticulum Stress in NECA-Induced Cardioprotection against IschemiaReperfusion Injury
المؤلفون المشاركون
Xing, Fengmei
Han, Hui
Zhang, Yidong
Jing, Liwei
Xu, Zhelong
Xi, Jinkun
He, Yonggui
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2017، العدد 2017 (31 ديسمبر/كانون الأول 2017)، ص ص. 1-10، 10ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2017-12-17
دولة النشر
مصر
عدد الصفحات
10
التخصصات الرئيسية
الملخص EN
Objective.
This study aimed to investigate whether the nonselective A2 adenosine receptor agonist NECA induces cardioprotection against myocardial ischemia/reperfusion (I/R) injury via glycogen synthase kinase 3β (GSK-3β) and the mitochondrial permeability transition pore (mPTP) through inhibition of endoplasmic reticulum stress (ERS).
Methods and Results.
H9c2 cells were exposed to H2O2 for 20 minutes.
NECA significantly prevented H2O2-induced TMRE fluorescence reduction, indicating that NECA inhibited the mPTP opening.
NECA blocked H2O2-induced GSK-3β phosphorylation and GRP94 expression.
NECA increased GSK-3β phosphorylation and decreased GRP94 expression, which were prevented by both ERS inductor 2-DG and PKG inhibitor KT5823, suggesting that NECA may induce cardioprotection through GSK-3β and cGMP/PKG via ERS.
In isolated rat hearts, both NECA and the ERS inhibitor TUDCA decreased myocardial infarction, increased GSK-3β phosphorylation, and reversed GRP94 expression at reperfusion, suggesting that NECA protected the heart by inhibiting GSK-3β and ERS.
Transmission electron microscopy showed that NECA and TUDCA reduced mitochondrial swelling and endoplasmic reticulum expansion, further supporting that NECA protected the heart by preventing the mPTP opening and ERS.
Conclusion.
These data suggest that NECA prevents the mPTP opening through inactivation of GSK-3β via ERS inhibition.
The cGMP/PKG signaling pathway is responsible for GSK-3β inactivation by NECA.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Xing, Fengmei& Han, Hui& He, Yonggui& Zhang, Yidong& Jing, Liwei& Xu, Zhelong…[et al.]. 2017. Roles of Endoplasmic Reticulum Stress in NECA-Induced Cardioprotection against IschemiaReperfusion Injury. Oxidative Medicine and Cellular Longevity،Vol. 2017, no. 2017, pp.1-10.
https://search.emarefa.net/detail/BIM-1194082
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Xing, Fengmei…[et al.]. Roles of Endoplasmic Reticulum Stress in NECA-Induced Cardioprotection against IschemiaReperfusion Injury. Oxidative Medicine and Cellular Longevity No. 2017 (2017), pp.1-10.
https://search.emarefa.net/detail/BIM-1194082
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Xing, Fengmei& Han, Hui& He, Yonggui& Zhang, Yidong& Jing, Liwei& Xu, Zhelong…[et al.]. Roles of Endoplasmic Reticulum Stress in NECA-Induced Cardioprotection against IschemiaReperfusion Injury. Oxidative Medicine and Cellular Longevity. 2017. Vol. 2017, no. 2017, pp.1-10.
https://search.emarefa.net/detail/BIM-1194082
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1194082
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر