Linked Life Data

10919987

Source:http://linkedlifedata.com/resource/pubmed/id/10919987

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-9-20
pubmed:abstractText
Transforming growth factor (TGF)-beta1 is an important regulator of inflammation and fibrosis. TGF-beta1 is usually secreted as a biologically latent protein called latent TGF-beta1 (L-TGF-beta1). L-TGF-beta1 has no biologic effect unless L-TGF-beta1 is converted to its active form. Using a well-recognized model of lung injury induced by the antineoplastic antibiotic bleomycin (Blm), we demonstrated that 7 d after intratracheal Blm administration, total lung TGF-beta was maximally increased. This induction was due to TGF-beta1 production by alveolar macrophages that, when explanted, generated increased quantities of L-TGF-beta1 complexed with the glycoprotein thrombospondin (TSP)-1. The TSP-1/L-TGF-beta1 complex was associated with CD36, a receptor for TSP-1. The association of TSP-1/L-TGF-beta1 to CD36 was critical for plasmin-mediated release of mature TGF-beta1. In this paper we show that, compared with administration of Blm by itself, when a synthetic peptide of CD36 between amino acids 93 and 110 is given concomitantly with Blm to rats, alveolar macrophages generate markedly less active TGF-beta1, the rats gain weight more rapidly, and there is less inflammation, collagen I and III, and fibronectin synthesis. These findings demonstrate a novel in vivo mechanism of activation of L-TGF-beta1 in lung injury and the importance of alveolar macrophage- derived active TGF-beta1 in the pathogenesis of pulmonary inflammation and fibrosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1044-1549
pubmed:author
pubmed:issnType
Print
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
204-12
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:10919987-Animals, pubmed-meshheading:10919987-Antigens, CD36, pubmed-meshheading:10919987-Bleomycin, pubmed-meshheading:10919987-Body Weight, pubmed-meshheading:10919987-Bronchoalveolar Lavage Fluid, pubmed-meshheading:10919987-Cell Count, pubmed-meshheading:10919987-Cell Survival, pubmed-meshheading:10919987-Collagen, pubmed-meshheading:10919987-Connective Tissue, pubmed-meshheading:10919987-Decorin, pubmed-meshheading:10919987-Extracellular Matrix Proteins, pubmed-meshheading:10919987-Female, pubmed-meshheading:10919987-Fibronectins, pubmed-meshheading:10919987-Inflammation, pubmed-meshheading:10919987-Lung, pubmed-meshheading:10919987-Lung Diseases, pubmed-meshheading:10919987-Macrophages, pubmed-meshheading:10919987-Oligopeptides, pubmed-meshheading:10919987-Proteoglycans, pubmed-meshheading:10919987-Rats, pubmed-meshheading:10919987-Rats, Sprague-Dawley, pubmed-meshheading:10919987-Transforming Growth Factor beta, pubmed-meshheading:10919987-Tumor Cells, Cultured
pubmed:year
2000
pubmed:articleTitle
A CD36 synthetic peptide inhibits bleomycin-induced pulmonary inflammation and connective tissue synthesis in the rat.
pubmed:affiliation
Departments of Internal Medicine and Pathology, and the Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Mannitoba, British Columbia, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't