Linked Life Data

15181371

Source:http://linkedlifedata.com/resource/pubmed/id/15181371

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2004-6-7
pubmed:abstractText
Ischemic preconditioning (IPC) promotes brain tolerance against subsequent ischemic insults. Using the organotypic hippocampal slice culture, we conducted the present study to investigate (1) the role of adenosine A1 receptor (A1AR) activation in IPC induction, (2) whether epsilon protein kinase C (epsilonPKC) activation after IPC is mediated by the phosphoinositol pathway, and (3) whether epsilonPKC protection is mediated by the extracellular signal-regulated kinase (ERK) pathway. Our results demonstrate that activation of A1AR emulated IPC, whereas blockade of the A1AR during IPC diminished neuroprotection. The neuroprotection promoted by the A1AR was also reduced by the epsilonPKC antagonist. To determine whether epsilonPKC activation in IPC and A1AR preconditioning is mediated by activation of the phosphoinositol pathway, we incubated slices undergoing IPC or adenosine treatment with a phosphoinositol phospholipase C inhibitor. In both cases, preconditioning neuroprotection was significantly attenuated. To further characterize the subsequent signal transduction pathway that ensues after epsilonPKC activation, mitogen-activated protein kinase kinase was blocked during IPC and pharmacologic preconditioning (PPC) (with epsilonPKC, NMDA, or A1AR agonists). This treatment significantly attenuated IPC- and PPC-induced neuroprotection. In conclusion, we demonstrate that epsilonPKC activation after IPC/PPC is essential for neuroprotection against oxygen/glucose deprivation in organotypic slice cultures and that the ERK pathway is downstream to epsilonPKC.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0271-678X
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
636-45
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:15181371-Animals, pubmed-meshheading:15181371-Animals, Newborn, pubmed-meshheading:15181371-Brain Ischemia, pubmed-meshheading:15181371-Enzyme Activation, pubmed-meshheading:15181371-Enzyme Inhibitors, pubmed-meshheading:15181371-Flavonoids, pubmed-meshheading:15181371-Hippocampus, pubmed-meshheading:15181371-Ischemic Preconditioning, pubmed-meshheading:15181371-Isoenzymes, pubmed-meshheading:15181371-MAP Kinase Signaling System, pubmed-meshheading:15181371-Mitogen-Activated Protein Kinases, pubmed-meshheading:15181371-Neurons, pubmed-meshheading:15181371-Protein Kinase C, pubmed-meshheading:15181371-Protein Kinase C-epsilon, pubmed-meshheading:15181371-Rats, pubmed-meshheading:15181371-Rats, Sprague-Dawley, pubmed-meshheading:15181371-Receptor, Adenosine A1, pubmed-meshheading:15181371-Receptors, Cell Surface
pubmed:year
2004
pubmed:articleTitle
Epsilon protein kinase C mediated ischemic tolerance requires activation of the extracellular regulated kinase pathway in the organotypic hippocampal slice.
pubmed:affiliation
Cerebral Vascular Disease Research Center, Department of Neurology and Neuroscience, University of Miami School of Medicine, Miami, Florida, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't