Post-ischemic activation of protein kinase C epsilon protects the hippocampus from cerebral ischemic injury via alterations in cerebral blood flow

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Abstract

Protein kinase C (PKC) is a family of serine/threonine-isozymes that are involved in many signaling events in normal and disease states. Previous studies from our lab have demonstrated that e{open}PKC plays a pivotal role in neuroprotection induced by ischemic preconditioning. However, the role of e{open}PKC during and after brain ischemia is not clearly defined. Therefore, in the present study, we tested the hypothesis that activation of e{open}PKC during an ischemic event is neuroprotective. Furthermore, other studies have demonstrated that e{open}PKC mediates cerebral ischemic tolerance in the rat brain by decreasing vascular tone. Thus, we also tested the effects of e{open}PKC activation during ischemia on cerebral blood flow (CBF). We found that ψe{open}-Receptors for Activated C Kinase (RACK), a e{open}PKC-selective peptide activator, injected intravenously 30. min before induction of global cerebral ischemia conferred neuroprotection in the CA1 region of the rat hippocampus. Moreover, measurements of CBF before, during, and after cerebral ischemia revealed a significant reduction in the reperfusion phase of rats pretreated with ψe{open}RACK as compared to Tat peptide (vehicle). Our results suggest that e{open}PKC can protect the rat brain against ischemic damage by regulating CBF. Thus, e{open}PKC may be one of the treatment modalities against ischemic injury.

Original languageEnglish
Pages (from-to)158-162
Number of pages5
JournalNeuroscience Letters
Volume487
Issue number2
DOIs
StatePublished - Jan 7 2011

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Cerebrovascular Circulation
Protein Kinase C-epsilon
Protein Kinase C
Hippocampus
Wounds and Injuries
Brain Ischemia
Ischemic Preconditioning
Peptides
Brain
Threonine
Serine
Isoenzymes
Reperfusion
Blood Vessels
Ischemia

Keywords

  • Cerebral blood flow
  • Epsilon protein kinase C
  • Ischemia
  • Neuroprotection

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

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title = "Post-ischemic activation of protein kinase C epsilon protects the hippocampus from cerebral ischemic injury via alterations in cerebral blood flow",
abstract = "Protein kinase C (PKC) is a family of serine/threonine-isozymes that are involved in many signaling events in normal and disease states. Previous studies from our lab have demonstrated that e{open}PKC plays a pivotal role in neuroprotection induced by ischemic preconditioning. However, the role of e{open}PKC during and after brain ischemia is not clearly defined. Therefore, in the present study, we tested the hypothesis that activation of e{open}PKC during an ischemic event is neuroprotective. Furthermore, other studies have demonstrated that e{open}PKC mediates cerebral ischemic tolerance in the rat brain by decreasing vascular tone. Thus, we also tested the effects of e{open}PKC activation during ischemia on cerebral blood flow (CBF). We found that ψe{open}-Receptors for Activated C Kinase (RACK), a e{open}PKC-selective peptide activator, injected intravenously 30. min before induction of global cerebral ischemia conferred neuroprotection in the CA1 region of the rat hippocampus. Moreover, measurements of CBF before, during, and after cerebral ischemia revealed a significant reduction in the reperfusion phase of rats pretreated with ψe{open}RACK as compared to Tat peptide (vehicle). Our results suggest that e{open}PKC can protect the rat brain against ischemic damage by regulating CBF. Thus, e{open}PKC may be one of the treatment modalities against ischemic injury.",
keywords = "Cerebral blood flow, Epsilon protein kinase C, Ischemia, Neuroprotection",
author = "{Della Morte}, David and Ami Raval and Dave, {Kunjan R} and {Wen Lin}, Hung and Miguel Perez-Pinzon",
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T1 - Post-ischemic activation of protein kinase C epsilon protects the hippocampus from cerebral ischemic injury via alterations in cerebral blood flow

AU - Della Morte, David

AU - Raval, Ami

AU - Dave, Kunjan R

AU - Wen Lin, Hung

AU - Perez-Pinzon, Miguel

PY - 2011/1/7

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N2 - Protein kinase C (PKC) is a family of serine/threonine-isozymes that are involved in many signaling events in normal and disease states. Previous studies from our lab have demonstrated that e{open}PKC plays a pivotal role in neuroprotection induced by ischemic preconditioning. However, the role of e{open}PKC during and after brain ischemia is not clearly defined. Therefore, in the present study, we tested the hypothesis that activation of e{open}PKC during an ischemic event is neuroprotective. Furthermore, other studies have demonstrated that e{open}PKC mediates cerebral ischemic tolerance in the rat brain by decreasing vascular tone. Thus, we also tested the effects of e{open}PKC activation during ischemia on cerebral blood flow (CBF). We found that ψe{open}-Receptors for Activated C Kinase (RACK), a e{open}PKC-selective peptide activator, injected intravenously 30. min before induction of global cerebral ischemia conferred neuroprotection in the CA1 region of the rat hippocampus. Moreover, measurements of CBF before, during, and after cerebral ischemia revealed a significant reduction in the reperfusion phase of rats pretreated with ψe{open}RACK as compared to Tat peptide (vehicle). Our results suggest that e{open}PKC can protect the rat brain against ischemic damage by regulating CBF. Thus, e{open}PKC may be one of the treatment modalities against ischemic injury.

AB - Protein kinase C (PKC) is a family of serine/threonine-isozymes that are involved in many signaling events in normal and disease states. Previous studies from our lab have demonstrated that e{open}PKC plays a pivotal role in neuroprotection induced by ischemic preconditioning. However, the role of e{open}PKC during and after brain ischemia is not clearly defined. Therefore, in the present study, we tested the hypothesis that activation of e{open}PKC during an ischemic event is neuroprotective. Furthermore, other studies have demonstrated that e{open}PKC mediates cerebral ischemic tolerance in the rat brain by decreasing vascular tone. Thus, we also tested the effects of e{open}PKC activation during ischemia on cerebral blood flow (CBF). We found that ψe{open}-Receptors for Activated C Kinase (RACK), a e{open}PKC-selective peptide activator, injected intravenously 30. min before induction of global cerebral ischemia conferred neuroprotection in the CA1 region of the rat hippocampus. Moreover, measurements of CBF before, during, and after cerebral ischemia revealed a significant reduction in the reperfusion phase of rats pretreated with ψe{open}RACK as compared to Tat peptide (vehicle). Our results suggest that e{open}PKC can protect the rat brain against ischemic damage by regulating CBF. Thus, e{open}PKC may be one of the treatment modalities against ischemic injury.

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