Linked Life Data

10905638

Source:http://linkedlifedata.com/resource/pubmed/id/10905638

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2000-12-20
pubmed:abstractText
Phospholipases A2 (PLA2s) regulate hydrolysis of fatty acids, including arachidonic acid, from the sn-2 position of phospholipid membranes. PLA2 activity has been implicated in neurotoxicity and neurodegenerative processes secondary to ischemia and reperfusion and other oxidative stresses. The PLA2s constitute a superfamily whose members have diverse functions and patterns of expression. A large number of PLA2s have been identified within the central nervous systems of rodents and humans. We postulated that group IV large molecular weight, cytosolic phospholipase A2 (cPLA2) has a unique role in neurotoxicity associated with ischemic or toxin stress. We created mice deficient in cPLA2 and tested this hypothesis in two injury models, ischemia/reperfusion and MPTP neurotoxicity. In each model cPLA2 deficient mice are protected against neuronal injury when compared to their wild type littermate controls. These experiments support the hypothesis that cPLA2 is an important mediator of ischemic and oxidative injuries in the brain.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0364-3190
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
745-53
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Phospholipases A2 in ischemic and toxic brain injury.
pubmed:affiliation
Anesthesia and Critical Care, Massachusetts General Hospital, Charlestown 02129, USA. sapirste@helix.mgh.harvard.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review