Linked Life Data

12529273

Source:http://linkedlifedata.com/resource/pubmed/id/12529273

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2003-1-16
pubmed:abstractText
Hepatocyte growth factor (HGF) is a renotropic protein that elicits antifibrogenic activity by preventing the activation of matrix-producing myofibroblast cells in animal models of chronic renal diseases. However, whether a delayed administration of HGF can still attenuate renal fibrosis remains uncertain. In this study, we examined the therapeutic potential of exogenous HGF on an established renal interstitial fibrosis induced by unilateral ureteral obstruction (UUO). Three days after UUO, the obstructed kidneys displayed interstitial fibrotic lesions with characteristic features of an established renal fibrosis, as manifested by myofibroblast activation, fibronectin overexpression, interstitial matrix deposition, and transforming growth factor-beta1 upregulation. Beginning at this time point, administration of recombinant HGF into mice by intravenous injections for 11 days markedly suppressed the progression of renal interstitial fibrosis. HGF significantly suppressed renal alpha-smooth muscle actin expression, total kidney collagen contents, interstitial matrix components, such as fibronectin, and renal expression of transforming growth factor-beta1 and its type I receptor. Compared with the starting point (3 days after UUO), HGF treatment largely blunted the progression of myofibroblast accumulation and collagen deposition but did not reverse it. Delayed administration of HGF also suppressed the myofibroblastic transdifferentiation from tubular epithelial cells in vitro, as demonstrated by a decline in alpha-smooth muscle actin and fibronectin expression. These results suggest that exogenous HGF exhibits potent therapeutic effects on retarding the progression of an established renal fibrosis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1931-857X
pubmed:author
pubmed:issnType
Print
pubmed:volume
284
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
F349-57
pubmed:dateRevised
2011-4-28
pubmed:meshHeading
pubmed-meshheading:12529273-Actins, pubmed-meshheading:12529273-Animals, pubmed-meshheading:12529273-Collagen, pubmed-meshheading:12529273-Disease Progression, pubmed-meshheading:12529273-Drug Administration Schedule, pubmed-meshheading:12529273-Fibroblasts, pubmed-meshheading:12529273-Fibronectins, pubmed-meshheading:12529273-Fibrosis, pubmed-meshheading:12529273-Hepatocyte Growth Factor, pubmed-meshheading:12529273-Kidney, pubmed-meshheading:12529273-Male, pubmed-meshheading:12529273-Mice, pubmed-meshheading:12529273-Mice, Inbred Strains, pubmed-meshheading:12529273-Muscle, Smooth, pubmed-meshheading:12529273-Recombinant Proteins, pubmed-meshheading:12529273-Transforming Growth Factor beta, pubmed-meshheading:12529273-Transforming Growth Factor beta1, pubmed-meshheading:12529273-Ureteral Obstruction
pubmed:year
2003
pubmed:articleTitle
Delayed administration of hepatocyte growth factor reduces renal fibrosis in obstructive nephropathy.
pubmed:affiliation
Division of Cellular and Molecular Pathology, Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't