Linked Life Data

18163956

Source:http://linkedlifedata.com/resource/pubmed/id/18163956

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2007-12-31
pubmed:abstractText
We previously reported that ONO-AE-248, a selective EP3 receptor agonist, has been shown to cause neutrophil death without the typical features of apoptosis and necrosis. However, the mechanism of the neutrophil death is unclear. By using Western blotting, flow cytometry (FACS) and confocal laser scanning microscopy (CLSM), we investigated the cellular signal transduction pathways of the neutrophil death. The research results showed that the neutrophil death induced by ONO-AE-248 did not show the morphologic changes of apoptosis and was not associated with the activity of caspase-3, caspase-8, and phosphorylation of p38-MAPK. However, impairment of mitochondria transmembrane potential has been found during the process of cell death. These findings suggested that ONO-AE-248 induced a non-apoptotic programmed cell death of neutrophils through partially mitochondria signaling transduction pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1672-7681
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
447-53
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Mitochondria play a role in the development of non-apoptotic programmed cell death of neutrophils induced by ONO-AE-248.
pubmed:affiliation
Laboratory of Molecular Biology, Department of Immunology, Luzhou Medical College, Luzhou, Sichuan 646000, China. jiajialiu08@hotmail.com
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't