We are analyzing https://link.springer.com/article/10.1007/s00395-017-0657-7.

Title:
The role of PI3Kα isoform in cardioprotection | Basic Research in Cardiology
Description:
Ischemic preconditioning (IPC) limits myocardial infarct size through the activation of the PI3K–Akt signal cascade; however, little is known about the roles of individual PI3K isoforms in cardioprotection. We aimed, therefore, to elucidate the role of the PI3Kα isoform in cardioprotection Pharmacological PI3Kα inhibition was assessed in isolated-perfused mouse hearts subjected to ischemia/reperfusion injury (IRI), either during the IPC procedure or at reperfusion. PI3Kα inhibition abrogated the IPC-induced protective effect at reperfusion, but not when given only during the IPC protocol. These results were confirmed in an in vivo model. Moreover, pharmacological PI3Kα activation by insulin at reperfusion was sufficient to confer cardioprotection against IRI. In addition, PI3Kα was shown to be expressed and activated in mouse cardiomyocytes, mouse cardiac endothelial cells, as well as in mouse and human heart tissue. Furthermore, PI3Kα was shown to mediate its effect though the inhibition of mitochondrial permeability transition pore opening. In conclusion, PI3Kα activity is required during the early reperfusion phase to reduce myocardial infarct size. This suggests that strategies specifically enhancing the α isoform of PI3K at reperfusion promote tissue salvage and as such, and could provide a direct target for clinical treatment of IRI.
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Keywords {🔍}

pikα, ipc, pubmed, article, reperfusion, google, scholar, insulin, mouse, heart, cas, myocardial, activation, tissue, gdcg, cardioprotection, role, human, akt, cardiomyocytes, preconditioning, pik, cells, min, protein, size, effect, cardiac, mptp, inhibition, protocol, cell, kinase, control, fig, ischemic, signalling, inhibitors, yellon, vivo, model, protection, infarct, endothelial, phosphorylation, activator, central, expression, iri, results,

Topics {✒️}

bio-rad mini trans-blot patient baseline characteristics article download pdf pro-survival signalling cascades mapping pro-survival cascades mouse langendorff-perfused hearts potassium–glucose–insulin solution glucose-insulin-potassium infusion intravenous glucose-insulin-potassium mann–whitney test depending parametric kruskal–wallis test ischaemic/reperfused heart—druggable related subjects 60 mg/kg sodium pentobarbitone university college london broad-spectrum pi3k inhibitors cardiac ischemia/reperfusion injury treat ischemia/reperfusion injury global ischemia-reperfusion injury pan-specific pi3k inhibitors full access pi3k isoform-specific agents involves gpcr-ligand activation baseline characteristics reactive oxygen species phosphate-buffered saline injected krebs–henseleit buffer hepes-based recording buffer reduced phosphoinositide 3-kinase acute myocardial infarction myocardial infarct size compensatory signalling pathways jonassen ak attenuate infarct size pi3kα-induced akt phosphorylation ros-mediated mptp model distinct pi3kα-selective inhibitors tyrosine kinase receptor rat hearts subjected phospho-threonine308 akt levels isoform-specific pi3k inhibitors privacy choices/manage cookies end-effector mechanism mediating promote myocardial salvage left ventricular tissue reporting animal research ros-stimulated mptp opening insulin-induced pi3kα activation article rossello cell signalling technology

Questions {❓}

Heusch G, Rassaf T (2016) Time to give up on cardioprotection?
Kleinbongard P, Heusch G (2015) Extracellular signalling molecules in the ischaemic/reperfused heart—druggable and translatable for cardioprotection?
Knight ZA, Gonzalez B, Feldman ME, Zunder ER, Goldenberg DD, Williams O, Loewith R, Stokoe D, Balla A, Toth B, Balla T, Weiss WA, Williams RL, Shokat KM (2006) A pharmacological map of the PI3-K family defines a role for p110?

Schema {🗺️}

WebPage:
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         headline:The role of PI3Kα isoform in cardioprotection
         description:Ischemic preconditioning (IPC) limits myocardial infarct size through the activation of the PI3K–Akt signal cascade; however, little is known about the roles of individual PI3K isoforms in cardioprotection. We aimed, therefore, to elucidate the role of the PI3Kα isoform in cardioprotection Pharmacological PI3Kα inhibition was assessed in isolated-perfused mouse hearts subjected to ischemia/reperfusion injury (IRI), either during the IPC procedure or at reperfusion. PI3Kα inhibition abrogated the IPC-induced protective effect at reperfusion, but not when given only during the IPC protocol. These results were confirmed in an in vivo model. Moreover, pharmacological PI3Kα activation by insulin at reperfusion was sufficient to confer cardioprotection against IRI. In addition, PI3Kα was shown to be expressed and activated in mouse cardiomyocytes, mouse cardiac endothelial cells, as well as in mouse and human heart tissue. Furthermore, PI3Kα was shown to mediate its effect though the inhibition of mitochondrial permeability transition pore opening. In conclusion, PI3Kα activity is required during the early reperfusion phase to reduce myocardial infarct size. This suggests that strategies specifically enhancing the α isoform of PI3K at reperfusion promote tissue salvage and as such, and could provide a direct target for clinical treatment of IRI.
         datePublished:2017-10-17T00:00:00Z
         dateModified:2017-10-17T00:00:00Z
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ScholarlyArticle:
      headline:The role of PI3Kα isoform in cardioprotection
      description:Ischemic preconditioning (IPC) limits myocardial infarct size through the activation of the PI3K–Akt signal cascade; however, little is known about the roles of individual PI3K isoforms in cardioprotection. We aimed, therefore, to elucidate the role of the PI3Kα isoform in cardioprotection Pharmacological PI3Kα inhibition was assessed in isolated-perfused mouse hearts subjected to ischemia/reperfusion injury (IRI), either during the IPC procedure or at reperfusion. PI3Kα inhibition abrogated the IPC-induced protective effect at reperfusion, but not when given only during the IPC protocol. These results were confirmed in an in vivo model. Moreover, pharmacological PI3Kα activation by insulin at reperfusion was sufficient to confer cardioprotection against IRI. In addition, PI3Kα was shown to be expressed and activated in mouse cardiomyocytes, mouse cardiac endothelial cells, as well as in mouse and human heart tissue. Furthermore, PI3Kα was shown to mediate its effect though the inhibition of mitochondrial permeability transition pore opening. In conclusion, PI3Kα activity is required during the early reperfusion phase to reduce myocardial infarct size. This suggests that strategies specifically enhancing the α isoform of PI3K at reperfusion promote tissue salvage and as such, and could provide a direct target for clinical treatment of IRI.
      datePublished:2017-10-17T00:00:00Z
      dateModified:2017-10-17T00:00:00Z
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      keywords:
         Cardioprotection
         Phosphoinositide 3-kinase
         Ischemic preconditioning
         Ischemia/reperfusion injury
         Cardiology
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               type:PostalAddress
            type:Organization
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            address:
               name:The Hatter Cardiovascular Institute, University College London, London, UK
               type:PostalAddress
            type:Organization
      name:Bart Vanhaesebroeck
      affiliation:
            name:University College London
            address:
               name:UCL Cancer Institute, University College London, London, UK
               type:PostalAddress
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      name:Sean M. Davidson
      affiliation:
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               name:The Hatter Cardiovascular Institute, University College London, London, UK
               type:PostalAddress
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      name:The Hatter Cardiovascular Institute, University College London, London, UK
      name:The Hatter Cardiovascular Institute, University College London, London, UK
      name:UCL Cancer Institute, University College London, London, UK
      name:The Hatter Cardiovascular Institute, University College London, London, UK
      name:The Hatter Cardiovascular Institute, University College London, London, UK

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