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Article: Smad3-mediated upregulation of miR-21 promotes renal fibrosis

TitleSmad3-mediated upregulation of miR-21 promotes renal fibrosis
Authors
Issue Date2011
Citation
Journal of the American Society of Nephrology, 2011, v. 22, n. 9, p. 1668-1681 How to Cite?
AbstractTGF-β/Smad signaling plays a role in fibrogenesis, but therapies targeting TGF-β are ineffective in treating renal fibrosis. Here, we explored the therapeutic potential of targeting TGF-β-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-β. Lack of Smad3, but not lack of Smad2, prevented cells from upregulating miR-21 in response to TGF-β. 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. Copyright © 2011 by the American Society of Nephrology.
Persistent Identifierhttp://hdl.handle.net/10722/199924
ISSN
2015 Impact Factor: 8.491
2015 SCImago Journal Rankings: 4.699
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZhong, Xiang-
dc.contributor.authorChung, Arthur Chi Kong-
dc.contributor.authorChen, Hai-Yong-
dc.contributor.authorMeng, Xiaoming-
dc.contributor.authorLan, Huiyao-
dc.date.accessioned2014-07-26T23:10:55Z-
dc.date.available2014-07-26T23:10:55Z-
dc.date.issued2011-
dc.identifier.citationJournal of the American Society of Nephrology, 2011, v. 22, n. 9, p. 1668-1681-
dc.identifier.issn1046-6673-
dc.identifier.urihttp://hdl.handle.net/10722/199924-
dc.description.abstractTGF-β/Smad signaling plays a role in fibrogenesis, but therapies targeting TGF-β are ineffective in treating renal fibrosis. Here, we explored the therapeutic potential of targeting TGF-β-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-β. Lack of Smad3, but not lack of Smad2, prevented cells from upregulating miR-21 in response to TGF-β. 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. Copyright © 2011 by the American Society of Nephrology.-
dc.languageeng-
dc.relation.ispartofJournal of the American Society of Nephrology-
dc.titleSmad3-mediated upregulation of miR-21 promotes renal fibrosis-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1681/ASN.2010111168-
dc.identifier.pmid21852586-
dc.identifier.scopuseid_2-s2.0-80052316668-
dc.identifier.hkuros232096-
dc.identifier.volume22-
dc.identifier.issue9-
dc.identifier.spage1668-
dc.identifier.epage1681-
dc.identifier.eissn1533-3450-
dc.identifier.isiWOS:000295705800015-

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