Source:http://linkedlifedata.com/resource/pubmed/id/11936776
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rdf:type | |
lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0016059,
umls-concept:C0017262,
umls-concept:C0040690,
umls-concept:C0043240,
umls-concept:C0185117,
umls-concept:C0273115,
umls-concept:C0332307,
umls-concept:C0374711,
umls-concept:C0443199,
umls-concept:C0597357,
umls-concept:C1705181,
umls-concept:C1707520,
umls-concept:C2709248,
umls-concept:C2911684
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pubmed:issue |
3
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pubmed:dateCreated |
2002-4-8
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pubmed:abstractText |
In a rat model of lung injury induced by the antineoplastic antibiotic, bleomycin, there is loss of type I alveolar epithelial cells (AECs) followed by infiltration of activated inflammatory cells, type II AEC proliferation, and fibrosis. At 4 and 7 days after bleomycin administration alveolar macrophages have increased production and release of active transforming growth factor (TGF)-beta1, an inhibitor of epithelial cell proliferation. Paradoxically at these same time intervals there is a concomitant induction of type II AEC proliferation. For TGF-beta-mediated signal transduction to occur, the expression of both TCF-beta receptor types I (TbetaR-I) and II (TbetaR-II) must be present. Using immunohistochemistry and in situ hybridization, 4 and 7 days after bleomycin administration the expression of TbetaR-I on AECs was reduced whereas that of TbetaR-II was unaltered. However, 14 and 28 days after bleomycin injury, when there is decreased proliferation and induction of differentiation of type II AECs, there was a return of TbetaR-I expression on AECs. In contrast, TbetaR-I and TbetaR-II were observed on interstitial fibroblasts at all time intervals after bleomycin administration. Because both TbetaR-I and TbetaR-II are required for signal transduction, the reduction of TbetaR-I levels on the alveolar epithelium may alter the sensitivity of AECs to the antiproliferative effects of TGF-beta1 present in increased quantities following bleomycin injury. The loss of an antiproliferative response to TGF-beta1 may be important for the regeneration of the alveolar epithelium by proliferation while the expression of both receptors onfibroblasts would result in TGF-1 signaling for the synthesis of connective tissue proteins. Ourfindings suggest that during bleomycin-induced pulmonary fibrosis, the effects of TGF-beta1 on cells may be regulated by the expression of TbetaRs.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Activin Receptors, Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Bleomycin,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Transforming Growth...,
http://linkedlifedata.com/resource/pubmed/chemical/TGF-beta type I receptor,
http://linkedlifedata.com/resource/pubmed/chemical/transforming growth factor-beta...
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pubmed:status |
MEDLINE
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pubmed:issn |
0190-2148
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
28
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
233-50
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:11936776-Activin Receptors, Type I,
pubmed-meshheading:11936776-Animals,
pubmed-meshheading:11936776-Bleomycin,
pubmed-meshheading:11936776-Cell Division,
pubmed-meshheading:11936776-Disease Models, Animal,
pubmed-meshheading:11936776-Epithelial Cells,
pubmed-meshheading:11936776-Female,
pubmed-meshheading:11936776-Gene Expression Regulation,
pubmed-meshheading:11936776-Lung,
pubmed-meshheading:11936776-Lung Diseases,
pubmed-meshheading:11936776-Protein-Serine-Threonine Kinases,
pubmed-meshheading:11936776-Pulmonary Fibrosis,
pubmed-meshheading:11936776-RNA, Messenger,
pubmed-meshheading:11936776-Rats,
pubmed-meshheading:11936776-Rats, Sprague-Dawley,
pubmed-meshheading:11936776-Receptors, Transforming Growth Factor beta,
pubmed-meshheading:11936776-Time Factors
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pubmed:articleTitle |
Differential expression of transforming growth factor-beta type I and II receptors by pulmonary cells in bleomycin-induced lung injury: correlation with repair and fibrosis.
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pubmed:affiliation |
Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Canada. nasreen.khalil@bccdc.hnet.bc.ca
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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