Linked Life Data

12969969

Source:http://linkedlifedata.com/resource/pubmed/id/12969969

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2003-12-19
pubmed:abstractText
Crosslinking of the antigen receptors on the immature B-cell lymphoma, WEHI-231, leads to growth arrest and apoptosis. Commitment to such B-cell receptor (BCR)-mediated apoptosis correlates with mitochondrial phospholipase A2 activation, disruption of mitochondrial function, and cathepsin B activation. CD40 signaling has been reported to rescue WEHI-231 B cells from BCR-driven apoptosis primarily via up-regulation of the antiapoptotic protein Bcl-xL. Coupling of the BCR to the mitochondrial phospholipase A2-dependent apoptotic pathway can be prevented by rescue signals via CD40. We now show that overexpression of Bcl-xL can prevent mitochondrial phospholipase A2 activation, disruption of mitochondrial potential, and postmitochondrial execution of BCR-mediated apoptosis via cathepsin B activation. Moreover, overexpression of Bcl-xL protects WEHI-231 B cells from mitochondrial disruption and apoptosis resulting from culture with exogenous arachidonic acid, the product of phospholipase A2 action, suggesting that Bcl-xL may act to antagonize arachidonic acid-mediated disruption of mitochondrial integrity. However, although Bcl-xL expression can mimic CD40-mediated rescue of BCR-driven apoptosis, it cannot substitute for CD40 signaling in the reversal of BCR-mediated growth arrest of WEHI-231 B cells. Rather, CD40 signaling additionally induces conversion of arachidonic acid to prostaglandin E2 (PGE2), which promotes WEHI-231 B-cell proliferation by restoring the sustained, cycling extracellular signal-regulated/mitogen-activated protein kinase (ErkMAPkinase) signaling required for cell cycle progression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
103
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
168-76
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:12969969-Animals, pubmed-meshheading:12969969-Antigens, CD40, pubmed-meshheading:12969969-Apoptosis, pubmed-meshheading:12969969-Arachidonic Acid, pubmed-meshheading:12969969-B-Lymphocytes, pubmed-meshheading:12969969-Cathepsin B, pubmed-meshheading:12969969-Cell Line, pubmed-meshheading:12969969-Enzyme Activation, pubmed-meshheading:12969969-Gene Expression, pubmed-meshheading:12969969-MAP Kinase Signaling System, pubmed-meshheading:12969969-Membrane Potentials, pubmed-meshheading:12969969-Mice, pubmed-meshheading:12969969-Mitochondria, pubmed-meshheading:12969969-Phospholipases A, pubmed-meshheading:12969969-Phospholipases A2, pubmed-meshheading:12969969-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:12969969-Receptors, Antigen, B-Cell, pubmed-meshheading:12969969-Signal Transduction, pubmed-meshheading:12969969-bcl-X Protein
pubmed:year
2004
pubmed:articleTitle
Bcl-(xL) antagonism of BCR-coupled mitochondrial phospholipase A(2) signaling correlates with protection from apoptosis in WEHI-231 B cells.
pubmed:affiliation
Division of Immunology, Infection and Inflammation, University of Glasgow, Glasgow, United Kingdom.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't