Linked Life Data

17786556

Source:http://linkedlifedata.com/resource/pubmed/id/17786556

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2007-10-1
pubmed:abstractText
Although ischemia-reperfusion (I/R) of small intestine is known to induce lung cell apoptosis, there is little information on intracellular and extracellular molecular mechanisms. Here, we investigated the mechanisms of apoptosis including the expression of Fas, Fas ligand (FasL), Bid, Bax, Bcl-2, cytochrome c, and activated caspase-3 in the rat lung at various time-points (0-24 h) of reperfusion after 1-h ischemia of small intestine. As assessed by TUNEL, the number of apoptotic epithelial cells, which were subsequently identified as type II alveolar epithelial cells by electron microscopy and immunohistochemical double-staining, increased at 3 h of reperfusion in the lung. However, intravenous injections of anti-TNF-alpha antibody decreased the number of TUNEL-positive cells, indicating involvement of tumor necrosis factor-alpha (TNF-alpha) in the induction of lung cell apoptosis. Western blotting and/or immunohistochemistry revealed a marked up-regulation of Fas, FasL, Bid, Bax, cytochrome c and activated caspase-3 and down-regulation of Bcl-2 in lung epithelial and stromal cells at 3 h of reperfusion. Our results indicate that I/R of small intestine results in apoptosis of rat alveolar type II cells through a series of events including systemic TNF-alpha, activation of two apoptotic signaling pathways and mitochondrial translocation of Bid.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1360-8185
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1989-2001
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Lung injury after ischemia-reperfusion of small intestine in rats involves apoptosis of type II alveolar epithelial cells mediated by TNF-alpha and activation of Bid pathway.
pubmed:affiliation
Department of Histology and Cell Biology, Unit of Basic Medical Science, Nagasaki University Graduate School of Biomedical Sciences, 1-12-4, Sakamoto, Nagasaki 852-8523, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't