Linked Life Data

16814783

Source:http://linkedlifedata.com/resource/pubmed/id/16814783

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
17
pubmed:dateCreated
2006-7-17
pubmed:abstractText
Epithelial-mesenchymal transition (EMT), a process whereby renal tubular epithelial cells lose phenotype and gain fibroblast-like characteristics, has been demonstrated to contribute significantly to the development of renal fibrosis. The immunosuppressant cyclosporine A (CsA) has been shown to induce renal fibrosis, a major complication of CsA therapy. The mechanisms that drive CsA-induced fibrosis remain undefined, however, CsA has been demonstrated to induce EMT in human renal proximal tubular epithelial cells (RPTEC). E2A transcription factors were identified as being upregulated by CsA treatment. To further examine the role of E2A proteins in EMT, E12 and E47 were overexpressed, alone and in combination, in human RPTEC. Both E12 and E47 elicited EMT effects on tubular epithelial cells with E47 more potent in inducing the fibroblast-like phenotype. These results indicate the important role of the E2A gene products in the progression of CsA-induced EMT and provide novel insights into CsA-induced renal fibrosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0014-5793
pubmed:author
pubmed:issnType
Print
pubmed:day
24
pubmed:volume
580
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4021-30
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Overexpression of E2A proteins induces epithelial-mesenchymal transition in human renal proximal tubular epithelial cells suggesting a potential role in renal fibrosis.
pubmed:affiliation
UCD School of Biomolecular and Biomedical Sciences, UCD Conway Institute, University College Dublin, Belfield, Dublin 4, Ireland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't