Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-7-9
pubmed:abstractText
We wondered whether the apoptosis known to occur after UV-B irradiation might involve the Fas/Fas ligand (FasL) signaling pathway. We exposed PBLs from normal individuals, and also the Jurkat (E6-1) and U937 cell lines, to graded doses of UV-B irradiation and observed a prompt and marked increase in Fas expression at doses as low as 0.5 mJ/cm2. Increased Fas expression did not require new protein synthesis, since cycloheximide-treated cells also showed an increase in Fas after UV-B. UV-B-irradiated cells cultured in the presence of zinc showed inhibition of apoptosis coincident with a marked increase in Fas+ cells, apparently indicating the accumulation of Fas-bearing cells unable to undergo apoptosis. After UV-B irradiation, PBLs showed increased expression of Fas ligand; the E6-1 lymphocytic cell line also released soluble FasL. UV-B induced apoptosis could be partially blocked by neutralizing FasL Abs, and a FasL-resistant variant of E6-1 cell line showed reduced apoptosis after UV-B irradiation, implying that the increase in Fas expression signified a role for Fas in UV-induced apoptosis. UV-induced Fas expression may serve to target stress-injured cells for removal by FasL-bearing cells or by FasL produced by the cells themselves in response to the stimuli, and may represent a general function of the Fas/FasL pathway in facilitating the apoptosis and elimination of undesirable or harmful cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
161
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
241-51
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:9647230-Adult, pubmed-meshheading:9647230-Antibodies, Monoclonal, pubmed-meshheading:9647230-Antigens, CD95, pubmed-meshheading:9647230-Apoptosis, pubmed-meshheading:9647230-Cell Survival, pubmed-meshheading:9647230-Cells, Cultured, pubmed-meshheading:9647230-Cycloheximide, pubmed-meshheading:9647230-Fas Ligand Protein, pubmed-meshheading:9647230-Humans, pubmed-meshheading:9647230-Immune Sera, pubmed-meshheading:9647230-Immunity, Innate, pubmed-meshheading:9647230-Jurkat Cells, pubmed-meshheading:9647230-Ligands, pubmed-meshheading:9647230-Lymphocytes, pubmed-meshheading:9647230-Lymphoma, Large B-Cell, Diffuse, pubmed-meshheading:9647230-Membrane Glycoproteins, pubmed-meshheading:9647230-Solubility, pubmed-meshheading:9647230-Tumor Cells, Cultured, pubmed-meshheading:9647230-Ultraviolet Rays, pubmed-meshheading:9647230-Zinc
pubmed:year
1998
pubmed:articleTitle
Fas/Fas ligand interactions are involved in ultraviolet-B-induced human lymphocyte apoptosis.
pubmed:affiliation
Department of Medicine, University of North Carolina at Chapel Hill 27599, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't