B-Type Natriuretic Peptide-Induced Cardioprotection against Reperfusion Is Associated with Attenuation of Mitochondrial Permeability Transition
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概要
- 論文の詳細を見る
B-type natriuretic peptide (BNP) is one peptide hormone released in response to myocyte stretch, whose functions play significant roles in health and disease. Its physiologic effects result in improved loading conditions and have led to the development of recombinant BNP as a therapeutic agent for heart failure. Previous work has identified that BNP protect myocardium against reperfusion injury through mitochondrial pathway. Mitochondria are both essential effectors of cardioprotection and primary targets of cardioprotective signaling. Their role during reperfusion is particularly critical because of the conditions that promote both apoptosis by the mitochondrial pathway and necrosis by irreversible damage to mitochondria in association with mitochondrial permeability transition pores (mPTP). After an episode of myocardial ischemia, opening of mPTP, at the onset of reperfusion, is a critical determinant of myocyte death. The relationship of BNP and mPTP in mediating reperfusion-induced cardiomyocytes injury is a novel investigative area. In this study, our results indicated that the beneficial effect of BNP in cultured cardiomyocytes subjected to reperfusion is associated with attenuation of mPTP opening, resultant mitochondrial dysfunction and apoptosis. Further investigation of underlying mechanisms revealed that these were associated with BNP-mediated repolarization of mitochondrial membrane potential (Δψm), inhibition of reactive oxygen species (ROS) generation, improvement of Bcl-2 level, and inhibition of Bax and second mitochondria-derived activator of caspases/direct inhibitor of apoptosis protein-binding protein with a low isoelectric point (Smac/DIABLO) levels. In summary, we demonstrate that BNP exerts protective actions within reperfusion by inhibiting mPTP opening and these roles of BNP may involve phosphatidylinositol 3-kinase (PI3K) dependent pathway.
- 日本薬学会の論文
著者
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ZHANG Yun
Department of Cardiology, Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese
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Yan Ming
Department Of Physiology Medical School Zhengzhou University
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Sun Yiguo
Department of Biomedical Engineering, Key Laboratory of Biomedical Engineering of Ministry of Educat
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Wu Yabin
Department of Biomedical Engineering, Key Laboratory of Biomedical Engineering of Ministry of Educat
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Zheng Xiaoxiang
Department of Biomedical Engineering, Key Laboratory of Biomedical Engineering of Ministry of Educat
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Zhang Yun
Department Of Biomedical Engineering Key Laboratory For Biomedical Engineering Of Ministry Of Educat
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Yan Ming
Department Of Orthopaedic Peking University Third Hospital
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Zheng Xiaoxiang
Department Of Biomedical Engineering Key Laboratory For Biomedical Engineering Of Ministry Of Educat
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Zheng Xiaoxiang
Department of Biomedical Engineering, Key Laboratory of Biomedical Engineering of Ministry of Education, Zhejiang University
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Wu Yabin
Department of Biomedical Engineering, Key Laboratory of Biomedical Engineering of Ministry of Education, Zhejiang University
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Zhang Yun
Department of Biomedical Engineering, Key Laboratory of Biomedical Engineering of Ministry of Education, Zhejiang University
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Sun Yiguo
Department of Biomedical Engineering, Key Laboratory of Biomedical Engineering of Ministry of Education, Zhejiang University
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Yan Ming
Department of Biomedical Engineering, Key Laboratory of Biomedical Engineering of Ministry of Education, Zhejiang University
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