Ischemic preconditioning via epsilon protein kinase C activation requires cyclooxygenase-2 activation in vitro.

Ischemic preconditioning via epsilon protein kinase C activation requires cyclooxygenase-2 activation in vitro. Research Abstract Details 

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Ischemic preconditioning via epsilon protein kinase C activation requires cyclooxygenase-2 activation in vitro. Abstract Text:

E Kim,A P Raval,R A Defazio,M A Perez-Pinzon,E Kim,A P Raval,R A Defazio,M A Perez-Pinzon,

The signaling pathway of cyclooxygenase-2 (COX-2) induction following ischemic preconditioning (IPC) in brain remains undefined. To determine role of COX-2 in ischemic preconditioning, we used two in vitro models: mixed cortical neuron/astrocyte cell cultures and organotypic hippocampal slice cultures. We simulated IPC by exposing cell or slice cultures to 1 h or 15 min of oxygen/glucose deprivation (OGD), respectively, 48 h prior to ischemia. To mimic ischemia in vitro, we exposed cell or slice cultures to OGD of 4 h or 40 min, respectively. In cell cultures, these experiments revealed that COX-2 induction peaked at 24 h following IPC in cell culture. Inhibition of COX-2 activation with 50 microM NS-398 (a COX-2 selective inhibitor) abolished IPC-mediated neuroprotection in both in vitro models. Next, we tested whether epsilon protein kinase C (epsilonPKC) and extracellular signal regulated kinase 1/2 (ERK1/2) activation was involved in IPC-mediated neuroprotection and COX-2 expression in cell culture. Cell cultures were treated with an epsilonPKC-specific activating peptide (psiepsilonRACK, 100 nM) for 1 h, and 48 h later were exposed to OGD. epsilonPKC activation increased ERK1/2 phosphorylation and COX-2 induction and conferred neuroprotection similar to IPC. Additionally, inhibition of either epsilonPKC or ERK1/2 activation abolished COX-2 expression and neuroprotection due to ischemic preconditioning. These results demonstrate a crucial role for the epsilonPKC-->ERK1/2-->COX-2 pathway in the induction of neuroprotection via ischemic preconditioning.

Ischemic preconditioning via epsilon protein kinase C activation requires cyclooxygenase-2 activation in vitro. Publishing Authors By Initials

E Kim,AP Raval,RA Defazio,MA Perez-Pinzon,E Kim,AP Raval,RA Defazio,MA Perez-Pinzon,

For similar surgical procedures, operative: cardiovascular surgical procedures: reperfusion research abstracts see: surgical procedures, operative: cardiovascular surgical procedures: reperfusion research

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Ischemic preconditioning via epsilon protein kinase C activation requires cyclooxygenase-2 activation in vitro. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Neuroscience

VOLUME: 145

Page Numbers: 931-41

Journal Abbreviation: Neuroscience

ISSN: 0306-4522

DAY: 20

MONTH: 02

YEAR: 2007

Ischemic preconditioning via epsilon protein kinase C activation requires cyclooxygenase-2 activation in vitro. Information

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LANGUAGE: eng

NlmUniqueID: 7605074

Ischemic preconditioning via epsilon protein kinase C activation requires cyclooxygenase-2 activation in vitro. Keywords Mesh Terms:

KEYWORDS: Reperfusion

MESH TERMS: metabolism

Chemical & Substance for Abstract: Ischemic preconditioning via epsilon protein kinase C activation requires cyclooxygenase-2 activation in vitro. Information

Substance Name: Protein Kinase C-epsilon

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for Ischemic preconditioning via epsilon protein kinase C activation requires cyclooxygenase-2 activation in vitro.

AFFILIATION: Cerebral Vascular Disease Research Center, Department of Neurology and Neuroscience Program, University of Miami Miller School of Medicine, Miami, FL 33101, USA.

Country: United States

AGENCY: United States NINDS

GRANT: NS34773

ACRONYM: NS

MEDLINETA: Neuroscience

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