Linked Life Data

21852586

Source:http://linkedlifedata.com/resource/pubmed/id/21852586

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2011-9-1
pubmed:abstractText
TGF-?/Smad signaling plays a role in fibrogenesis, but therapies targeting TGF-? are ineffective in treating renal fibrosis. Here, we explored the therapeutic potential of targeting TGF-?-induced microRNA in the progression of renal fibrosis. Microarray analysis and real-time PCR revealed upregulation of miR-21 in tubular epithelial cells (TECs) in response to TGF-?. Lack of Smad3, but not lack of Smad2, prevented cells from upregulating miR-21 in response to TGF-?. In addition, Smad3-deficient mice were protected from upregulation of miR-21 and fibrosis in the unilateral ureteral obstruction model. In contrast, conditional knockout of Smad2 enhanced miR-21 expression and renal fibrosis. Furthermore, ultrasound-microbubble-mediated gene transfer of a miR-21-knockdown plasmid halted the progression of renal fibrosis in established obstructive nephropathy. In conclusion, these data demonstrate that Smad3, but not Smad2, signaling increases expression of miR-21, which promotes renal fibrosis. Inhibition of miR-21 may be a therapeutic approach to suppress renal fibrosis.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1533-3450
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1668-81
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Smad3-mediated upregulation of miR-21 promotes renal fibrosis.
pubmed:affiliation
Li Ka Shing Institute of Health Sciences, Department of Chemical Pathology, The Chinese University of Hong Kong, Hong Kong, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't