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Complete loss of ischaemic preconditioning-induced cardioprotection in mice with partial deficiency of HIF-1{alpha}.

Complete loss of ischaemic preconditioning-induced cardioprotection in mice with partial deficiency of HIF-1{alpha}. Research Abstract Details 

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  • Complete loss of ischaemic preconditioning-induced cardioprotection in mice with partial deficiency of HIF-1{alpha}. Abstract Text:

    zheqing caiZheqing Cai,hua zhongHua Zhong,marta bosch-marceMarta Bosch-Marce,karen fox-talbotKaren Fox-Talbot,lei wangLei Wang,chiming weiChiming Wei,michael a trushMichael A Trush,gregg l semenzaGregg L Semenza,zheqing caiZheqing Cai,hua zhongHua Zhong,marta bosch-marceMarta Bosch-Marce,karen fox-talbotKaren Fox-Talbot,lei wangLei Wang,chiming weiChiming Wei,michael a trushMichael A Trush,gregg l semenzaGregg L Semenza,

    AIMS: We investigated whether hypoxia-inducible factor 1alpha (HIF-1alpha) plays a role in the acute phase of ischaemic preconditioning (IPC). METHODS AND RESULTS: Hearts from wild-type (WT) mice and mice heterozygous for a null allele at the locus encoding HIF-1alpha (HET) were subjected to IPC (10-min ischaemia/5 min reperfusion, or two cycles of 5 min ischaemia/5 min reperfusion), followed by 30 min ischaemia and reperfusion. Left ventricular-developed pressure, heart rate, and coronary flow rate were measured continuously. Apoptosis and infarct size were assessed by TUNEL assay, cleaved caspase 3 immunohistochemistry, and triphenyltetrazolium chloride staining. Production of reactive oxygen species (ROS) in isolated cardiac mitochondria was measured by a chemiluminescence assay. The phosphatase and tensin homologue (PTEN) and AKT (protein kinase B) were analysed by immunoblot assay. IPC improved functional recovery and limited infarct size and apoptosis after prolonged ischaemia-reperfusion in WT hearts, but not in HET hearts. Mitochondrial ROS production, PTEN oxidation, and AKT phosphorylation were impaired in HET hearts. WT and HET hearts were protected by adenosine, which acts via an ROS-independent mechanism. CONCLUSION: HIF-1alpha is required for IPC-induced mitochondrial ROS production and myocardial protection against ischaemia-reperfusion injury.

    Complete loss of ischaemic preconditioning-induced cardioprotection in mice with partial deficiency of HIF-1{alpha}. Publishing Authors By Initials

    z caiZ Cai,h zhongH Zhong,m bosch-marceM Bosch-Marce,k fox-talbotK Fox-Talbot,l wangL Wang,c weiC Wei,ma trushMA Trush,gl semenzaGL Semenza,z caiZ Cai,h zhongH Zhong,m bosch-marceM Bosch-Marce,k fox-talbotK Fox-Talbot,l wangL Wang,c weiC Wei,ma trushMA Trush,gl semenzaGL Semenza,

    For similar abstracts research abstracts see: abstracts research

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    Complete loss of ischaemic preconditioning-induced cardioprotection in mice with partial deficiency of HIF-1{alpha}. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: Cardiovascular research

    VOLUME: 77

    Page Numbers: 463-70

    Journal Abbreviation: Cardiovasc. Res.

    ISSN: 0008-6363

    DAY: 11

    MONTH: 10

    YEAR: 2007

    Complete loss of ischaemic preconditioning-induced cardioprotection in mice with partial deficiency of HIF-1{alpha}. Information

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    LANGUAGE: eng

    NlmUniqueID: 77427

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    Grant and Affiliation Information for Complete loss of ischaemic preconditioning-induced cardioprotection in mice with partial deficiency of HIF-1{alpha}.

    AFFILIATION: Vascular Program, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

    Country: Netherlands

    Netherlands Research PublicationNetherlands Research Publication

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    MEDLINETA: Cardiovasc Res

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