AMP-Activated Protein Kinase Activation during Cardioplegia-Induced HypoxiaReoxygenation Injury Attenuates Cardiomyocytic Apoptosis via Reduction of Endoplasmic Reticulum Stress
Joint Authors
Fang, Shu-Wen
Chen, Tzu-Ping
Yeh, Chi-Hsiao
Lin, Yu-Min
Wang, Yao-Chang
Source
Issue
Vol. 2010, Issue 2010 (31 Dec. 2010), pp.1-9, 9 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2011-01-23
Country of Publication
Egypt
No. of Pages
9
Main Subjects
Abstract EN
Cardioplegic-induced H/R injury results in cardiomyocytic apoptosis.
AMPK has been shown to reduce ER stress and the unfolded protein response (UPR).
Whether AMPK activation can attenuate cardiomyocytic apoptosis after cardioplegia-induced H/R injury is unknown.
Cardiomyocytes were exposed to simulated ischemia by incubation in a hypoxic chamber with intermittent cold cardioplegia solution infusion at 20-minute intervals and subsequently reoxygenated in a normoxic environment.
Various doses of AMPK activators (AICAR or metformin) were given 2 days before H/R injury.
The cardiomyocytes were harvested after reoxygenation for subsequent examination.
With both AMPK activators, the antiapoptotic genes of ER stress and UPR, the subsequent production of proapoptotic proteins was attenuated, and the antiapoptotic proteins were elevated.
The activity of the apoptotic effectors of ER stress was also reduced with AMPK activation.
Moreover, TUNEL staining showed that AMPK activation significantly reduced the percentage of apoptotic cardiomyocytes after cardioplegia-induced H/R injury.
Our results revealed that AMPK activation during cardioplegia-induced H/R injury attenuates cardiomyocytic apoptosis, via enhancement of antiapoptotic and reduction of proapoptotic responses, resulting from lessening ER stress and the UPR.
AMPK activation may serve as a future pharmacological target to reduce H/R injury in the clinical setting.
American Psychological Association (APA)
Yeh, Chi-Hsiao& Chen, Tzu-Ping& Wang, Yao-Chang& Lin, Yu-Min& Fang, Shu-Wen. 2011. AMP-Activated Protein Kinase Activation during Cardioplegia-Induced HypoxiaReoxygenation Injury Attenuates Cardiomyocytic Apoptosis via Reduction of Endoplasmic Reticulum Stress. Mediators of Inflammation،Vol. 2010, no. 2010, pp.1-9.
https://search.emarefa.net/detail/BIM-448103
Modern Language Association (MLA)
Yeh, Chi-Hsiao…[et al.]. AMP-Activated Protein Kinase Activation during Cardioplegia-Induced HypoxiaReoxygenation Injury Attenuates Cardiomyocytic Apoptosis via Reduction of Endoplasmic Reticulum Stress. Mediators of Inflammation No. 2010 (2010), pp.1-9.
https://search.emarefa.net/detail/BIM-448103
American Medical Association (AMA)
Yeh, Chi-Hsiao& Chen, Tzu-Ping& Wang, Yao-Chang& Lin, Yu-Min& Fang, Shu-Wen. AMP-Activated Protein Kinase Activation during Cardioplegia-Induced HypoxiaReoxygenation Injury Attenuates Cardiomyocytic Apoptosis via Reduction of Endoplasmic Reticulum Stress. Mediators of Inflammation. 2011. Vol. 2010, no. 2010, pp.1-9.
https://search.emarefa.net/detail/BIM-448103
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-448103