Linked Life Data

9378990

Source:http://linkedlifedata.com/resource/pubmed/id/9378990

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1997-11-7
pubmed:abstractText
As an extension of the observation that mast cells undergo apoptosis following growth factor deprivation, we hypothesized that mast cells might also undergo apoptosis in response to activation through Fas Ag (CD95, APO-1), thus providing an additional pathway that could contribute to the regulation of mast cell numbers. Surface expression of Fas Ag was studied by flow cytometry, and apoptotic changes following treatment with anti-Fas mAb were analyzed using flow cytometric analysis of PI uptake and TUNEL staining, DNA electrophoresis, and electron microscopy. Murine bone marrow-cultured mast cells (BMCMC) and peritoneal mast cells, as well as two mast cell lines (C57 and MCP-5), constitutively expressed Fas Ag. Aggregation of Fas Ag with anti-Fas mAb resulted in the characteristic changes of apoptosis in C57 mast cells. BMCMC were resistant to anti-Fas mAb alone, but after the addition of actinomycin D also exhibited apoptosis in response to anti-Fas treatment. In addition, actinomycin D alone induced apoptosis. Stem cell factor, TGF-beta, and Fc epsilon RI aggregation enhanced Fas expression. However, Fas-mediated apoptosis was not augmented by Fc epsilon RI aggregation, and stem cell factor and TGF-beta partially protected BMCMC against Fas-mediated cytotoxicity. Finally, C57 mast cells were highly susceptible to killing by a Fas ligand-bearing CTL hybridoma, while BMCMC were relatively resistant, consistent with the results using anti-Fas mAb. Thus, induction of mast cell apoptosis by activation of the Fas pathway provides an additional mechanism by which mast cell numbers may be regulated in biologic systems.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
159
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4006-14
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9378990-Animals, pubmed-meshheading:9378990-Antibodies, Monoclonal, pubmed-meshheading:9378990-Antigens, CD95, pubmed-meshheading:9378990-Apoptosis, pubmed-meshheading:9378990-Cell Line, pubmed-meshheading:9378990-Cell Survival, pubmed-meshheading:9378990-Chromium Radioisotopes, pubmed-meshheading:9378990-Coculture Techniques, pubmed-meshheading:9378990-Cross-Linking Reagents, pubmed-meshheading:9378990-Dactinomycin, pubmed-meshheading:9378990-Fas Ligand Protein, pubmed-meshheading:9378990-Hybridomas, pubmed-meshheading:9378990-Ligands, pubmed-meshheading:9378990-Mast Cells, pubmed-meshheading:9378990-Membrane Glycoproteins, pubmed-meshheading:9378990-Mice, pubmed-meshheading:9378990-Mice, Inbred BALB C, pubmed-meshheading:9378990-Mice, Inbred MRL lpr, pubmed-meshheading:9378990-Receptors, IgE, pubmed-meshheading:9378990-T-Lymphocytes, Cytotoxic
pubmed:year
1997
pubmed:articleTitle
Fas (CD95, APO-1) antigen expression and function in murine mast cells.
pubmed:affiliation
Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't