Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2004-2-23
pubmed:abstractText
CD44 is a glycoprotein involved in inflammation and cell-cell/cell-matrix interactions. CD44 is upregulated in the kidney upon injury; however, its role in the pathogenesis of renal damage and fibrosis remains largely unknown. The authors show that mice lacking CD44 developed more tubular damage, associated with decreased proliferation and increased apoptosis of tubular epithelial cells, but less renal fibrosis after unilateral ureteral obstruction. In addition, impaired influx of macrophages and decreased accumulation of myofibroblasts was observed in the obstructed kidney of CD44(-/-) mice compared with CD44(+/+) mice. Hepatocyte growth factor (HGF) and transforming growth factor-beta1 (TGF-beta1) exert reciprocal functions in the progression of renal diseases and interact with CD44 in vitro. For the first time, the authors establish diminished HGF-signaling, via its high affinity receptor c-Met, in the absence of CD44 in vivo. In parallel, the signaling of TGF-beta1 reflected by the relative phosphorylation and nuclear translocation of Smad-2 and Smad-3 was reduced in the obstructed kidney of CD44(-/-) mice. In conclusion, CD44 exerts protective effects on tubuli but contributes to renal fibrogenesis at least in part through enhancement of HGF and TGF-beta1 signaling pathway in obstructive nephropathy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1046-6673
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
674-86
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
CD44 deficiency increases tubular damage but reduces renal fibrosis in obstructive nephropathy.
pubmed:affiliation
Departments of Pathology and Surgery, Academic Medical Center, Amsterdam, The Netherlands. k.m.rouschop@amc.uva.nl
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't