rdf:type |
|
lifeskim:mentions |
umls-concept:C0014597,
umls-concept:C0015127,
umls-concept:C0024109,
umls-concept:C0026336,
umls-concept:C0026473,
umls-concept:C0086418,
umls-concept:C0162638,
umls-concept:C0242488,
umls-concept:C0253023,
umls-concept:C0391871,
umls-concept:C1314792,
umls-concept:C1533691,
umls-concept:C1879547
|
pubmed:issue |
3
|
pubmed:dateCreated |
2008-3-3
|
pubmed:abstractText |
Alveolar epithelial cell death plays a crucial role in the progression of acute lung injury. We have demonstrated up-regulation of Fas expression on alveolar epithelial cells, and soluble Fas ligand secretion from inflammatory cells upon acute lung injury. Here we show that the lipopolysaccharide-stimulated human monocyte cell line THP-1 releases Fas ligand, and that conditioned medium from lipopolysaccharide-stimulated THP-1 cells induces apoptosis of the human pulmonary adenocarcinoma cell line A549. Activation of caspase-3 and -8 is associated with the apoptosis. Gene targeting on Fas in A549 cells by specific small interfering RNA impairs apoptosis induced by conditioned medium from activated THP-1, while that on Fas ligand in THP-1 cells impairs the apoptosis-inducing activity of the conditioned medium produced by lipopolysaccharide-stimulated cells. These results suggest that Fas ligand released by monocytes causes alveolar epithelial cell death through a Fas-dependent apoptotic mechanism in the development of acute lung injury.
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Mar
|
pubmed:issn |
0918-6158
|
pubmed:author |
pubmed-author:AmayaFumimasaF,
pubmed-author:HashimotoSatoruS,
pubmed-author:HashimotoSoshiS,
pubmed-author:IshizakaAkitoshiA,
pubmed-author:KitamuraYoshihiroY,
pubmed-author:KohHidefumiH,
pubmed-author:MagaeJunjiJ,
pubmed-author:MatsuyamaHirokiH,
pubmed-author:MizutaMitsuhikoM,
pubmed-author:MizutaNaruhikoN,
pubmed-author:NakajimaHirooH,
pubmed-author:NakajimaYasufumiY,
pubmed-author:ShimeNobuakiN,
pubmed-author:TanumaSei-ichSI
|
pubmed:issnType |
Print
|
pubmed:volume |
31
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
386-90
|
pubmed:meshHeading |
pubmed-meshheading:18310897-Acute Disease,
pubmed-meshheading:18310897-Antigens, CD95,
pubmed-meshheading:18310897-Apoptosis,
pubmed-meshheading:18310897-Cell Line, Tumor,
pubmed-meshheading:18310897-Culture Media, Conditioned,
pubmed-meshheading:18310897-Epithelial Cells,
pubmed-meshheading:18310897-Fas Ligand Protein,
pubmed-meshheading:18310897-Humans,
pubmed-meshheading:18310897-Lipopolysaccharides,
pubmed-meshheading:18310897-Lung,
pubmed-meshheading:18310897-Lung Diseases,
pubmed-meshheading:18310897-Monocytes,
pubmed-meshheading:18310897-RNA, Small Interfering,
pubmed-meshheading:18310897-RNA Interference,
pubmed-meshheading:18310897-Transfection
|
pubmed:year |
2008
|
pubmed:articleTitle |
Fas ligand released by activated monocytes causes apoptosis of lung epithelial cells in human acute lung injury model in vitro.
|
pubmed:affiliation |
Department of Anesthesiology and Intensive Care, Kyoto Prefectural University of Medicine, 465 Kajiicho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602-8566, Japan.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|