PKC-ε is upstream and PKC-α is downstream of mitoKATP channels in the signal transduction pathway of ischemic preconditioning of human myocardium

@article{Hassouna2004PKCIU,
  title={PKC-$\epsilon$ is upstream and PKC-$\alpha$ is downstream of mitoKATP channels in the signal transduction pathway of ischemic preconditioning of human myocardium},
  author={Ashraf Hamed Hassouna and Bashir Mnene Matata and Manuel Gali{\~n}anes},
  journal={American Journal of Physiology-cell Physiology},
  year={2004},
  volume={287}
}
Protein kinase C (PKC) is involved in the process of ischemic preconditioning (IPC), although the precise mechanism is still a subject of debate. Using specific PKC inhibitors, we investigated whic... 

Diazoxide acts more as a PKC‐ɛ activator, and indirectly activates the mitochondrial KATP channel conferring cardioprotection against hypoxic injury

This work aimed to clarify the role of PKC isoforms and the relationship between the PKCISO forms and the mitoKATP channel in diazoxide‐induced cardioprotection.

Mitochondrial ATP-sensitive potassium channels and mitochondrial protein kinase C: sometimes it's good to have a close neighbor.

  • G. Grover
  • Biology
    American journal of physiology. Heart and circulatory physiology
  • 2006
The fine study by Jiang et al. is an important milestone in the ongoing studies on the role of the mitochondrial ATP-sensitive K+ (mitoKATP) channels in myocardial ischemia.

Signaling pathways involved in postconditioning-induced cardioprotection of human myocardium, in vitro

In conclusion, PKC activation, opening of mitoKATP channels and p38 MAPK activation in early reoxygenation induced the postconditioning of human myocardium, in vitro.

Signaling Mechanisms in Ischemic Preconditioning: Interaction of PKCε and MitoKATP in the Inner Membrane of Mitochondria

IPC is a process in which brief periods of ischemia improves the ability of the heart to tolerate subsequent prolonged ischemic periods, and the opening of a mitochondrial channel is believed to be critical for the induction of IPC.

Protein kinase C subtypes and retinal ischemic preconditioning.

Sevoflurane-induced cardioprotection depends on PKC-alpha activation via production of reactive oxygen species.

Sevoflurane improves post-ischaemic contractile recovery via activation of PKC-alpha, and ROS production, but not opening of mitoK+(ATP) channels, precedes PKc-alpha translocation towards mitochondria.

Selective blockade of protein kinase B protects the rat and human myocardium against ischaemic injury

In conclusion, inhibition of PKB plays a critical role in protection of the mammalian myocardium and may represent a clinical target for the reduction of ischaemic injury.
...

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Opening of mitochondrial KATP channel occurs downstream of PKC-ε activation in the mechanism of preconditioning

We examined whether the mitochondrial ATP-sensitive K channel (KATP) is an effector downstream of protein kinase C-e (PKC-e) in the mechanism of preconditioning (PC) in isolated rabbit hearts. PC w...

Protein Kinase C- ξ is Responsible for the Protection of Preconditioning in Rabbit Cardiomyocytes

It is indicated that PKC-epsilon alone is responsible for the early phase of PC's protection in rabbit cardiomyocytes and this study uses novel peptide inhibitors which correspond to part of the amino acid sequence from the isozyme-specific RACK-binding site on the PKC molecule.

Downregulation of Protein Kinase C Inhibits Activation of Mitochondrial KATP Channels by Diazoxide

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It is concluded that ischemic preconditioning activates PKC-alpha, and thus ecto-5'-nucleotidase, in the preconditionsed myocardium and this enhancement was blunted by GF109203X.

PKC-δ inhibition does not block preconditioning-induced preservation in mitochondrial ATP synthesis and infarct size reduction in rats

It is demonstrated, using a luciferase-based assay to determine the rate of ATP synthesis and state of mitochondrial bioenergetics, that IPC preserves ATP synthesis in the ischemic myocardium and that this preservation is attenuated by the isoform non-selective PKC inhibitor, chelerythrine, but not by the δ- selective antagonist, rottlerin.

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Pharmacological and ischemic preconditioning of the human myocardium: mitoKATP channels are upstream and p38MAPK is downstream of PKC

Opening of mitoKATP channels and activation of PKC and p38MAPK are obligatory steps in the signal transduction cascade of IP and PP of the human myocardium with PKC activation being downstream of the opening of mkinase kinase channels and upstream of p38 MAPK activation.

Preconditioning of isolated rat heart is mediated by protein kinase C.

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