Linked Life Data

15591043

Source:http://linkedlifedata.com/resource/pubmed/id/15591043

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2005-2-28
pubmed:abstractText
In the kidney, a unique plasticity exists between epithelial and mesenchymal cells. During kidney development, the metanephric mesenchyme contributes to emerging epithelium of the nephron via mesenchymal to epithelial transition (MET). In the injured adult kidney, renal epithelia contribute to the generation of fibroblasts via epithelial-mesenchymal transition, facilitating renal fibrosis. Recombinant human bone morphogenic protein (BMP)-7, a morphogen that is essential for the conversion of epithelia from condensing mesenchyme during kidney development, enhances the repair of tubular structures in the kidney. In this setting, BMP-7 inhibits epithelial-mesenchymal transition involving adult renal epithelial tubular cells and decreases secretion of type I collagen by adult renal fibroblasts. In search of a mechanism behind the ability of BMP-7 to repair damaged renal tubules, we hypothesized that systemic treatment with BMP-7 might induce MET involving adult renal fibroblasts in the injured kidney, generating functional epithelial cells. Here we report that BMP-7 induces formation of epithelial cell aggregates in adult renal fibroblasts associated with reacquisition of E-cadherin expression and decreased motility, mimicking the effect of BMP-7 on embryonic metanephric mesenchyme to generate epithelium. In addition, we provide evidence that BMP-7-mediated repair of renal injury is associated with MET involving adult renal interstitial fibroblasts in mouse models for renal fibrosis. Collectively, these findings suggest that adult renal fibroblasts might retain parts of their original embryonic imprint and plasticity, which can be re-engaged by systemic administration of BMP-7 to mediate repair of tubular injury in a fibrotic kidney.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
4
pubmed:volume
280
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
8094-100
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:15591043-Animals, pubmed-meshheading:15591043-Bone Morphogenetic Protein 7, pubmed-meshheading:15591043-Bone Morphogenetic Proteins, pubmed-meshheading:15591043-Cadherins, pubmed-meshheading:15591043-Cell Movement, pubmed-meshheading:15591043-Cell Proliferation, pubmed-meshheading:15591043-Collagen Type I, pubmed-meshheading:15591043-Epithelial Cells, pubmed-meshheading:15591043-Fibroblasts, pubmed-meshheading:15591043-Humans, pubmed-meshheading:15591043-Immunohistochemistry, pubmed-meshheading:15591043-Kidney, pubmed-meshheading:15591043-Mesoderm, pubmed-meshheading:15591043-Mice, pubmed-meshheading:15591043-Nephritis, pubmed-meshheading:15591043-Promoter Regions, Genetic, pubmed-meshheading:15591043-Protein Structure, Tertiary, pubmed-meshheading:15591043-Recombinant Proteins, pubmed-meshheading:15591043-Regeneration, pubmed-meshheading:15591043-Sepharose, pubmed-meshheading:15591043-Time Factors, pubmed-meshheading:15591043-Transforming Growth Factor beta
pubmed:year
2005
pubmed:articleTitle
Bone morphogenic protein-7 induces mesenchymal to epithelial transition in adult renal fibroblasts and facilitates regeneration of injured kidney.
pubmed:affiliation
Center for Matrix Biology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't