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Article: Smad7 transgene attenuates peritoneal fibrosis in uremic rats treated with peritoneal dialysis

TitleSmad7 transgene attenuates peritoneal fibrosis in uremic rats treated with peritoneal dialysis
Authors
Issue Date2007
PublisherAmerican Society of Nephrology. The Journal's web site is located at http://www.jasn.org
Citation
Journal Of The American Society Of Nephrology, 2007, v. 18 n. 10, p. 2689-2703 How to Cite?
AbstractTransforming growth factor β (TGF-β) plays a critical role in the pathogenesis of the peritoneal fibrosis that complicates long-term peritoneal dialysis (PD). We studied the TGF-β/Smad signaling pathway in peritoneal fibrosis induced in uremic rats treated with PD and explored the therapeutic potential of Smad7 to prevent fibrogenesis. After subtotal nephrectomy, uremic rats were treated with peritoneal dialysis using 4.25% dextrose-containing fluid. The peritoneum of uremic rats treated with PD demonstrated fibrosis, increased TGF-β expression, increased Smad2/3 activation, decreased Smad7 expression, and increased expression of fibrogenic and angiogenic factors. In addition, peritoneal function was impaired and its structure was altered, including a thickened submesothelial layer. In rats transfected with a Smad7 transgene using an ultrasound-microbubble-mediated system, peritoneal fibrosis was attenuated, peritoneal function was improved, and Smad2/3 activation was inhibited. We suggest that administration of Smad7 inhibits peritoneal fibrogenesis in uremic rats treated with PD by correcting the imbalance between downregulated Smad7 and activated Smad2/3. Blockade of the TGF-β/Smad signaling pathway may represent a novel therapeutic approach to prevent peritoneal fibrosis in patients treated with PD. Copyright © 2007 by the American Society of Nephrology.
Persistent Identifierhttp://hdl.handle.net/10722/163116
ISSN
2015 Impact Factor: 8.491
2015 SCImago Journal Rankings: 4.699
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorGuo, Hen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorLam, MFen_HK
dc.contributor.authorChan, LYYen_HK
dc.contributor.authorTsang, AWLen_HK
dc.contributor.authorLan, HYen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2012-09-05T05:27:49Z-
dc.date.available2012-09-05T05:27:49Z-
dc.date.issued2007en_HK
dc.identifier.citationJournal Of The American Society Of Nephrology, 2007, v. 18 n. 10, p. 2689-2703en_HK
dc.identifier.issn1046-6673en_HK
dc.identifier.urihttp://hdl.handle.net/10722/163116-
dc.description.abstractTransforming growth factor β (TGF-β) plays a critical role in the pathogenesis of the peritoneal fibrosis that complicates long-term peritoneal dialysis (PD). We studied the TGF-β/Smad signaling pathway in peritoneal fibrosis induced in uremic rats treated with PD and explored the therapeutic potential of Smad7 to prevent fibrogenesis. After subtotal nephrectomy, uremic rats were treated with peritoneal dialysis using 4.25% dextrose-containing fluid. The peritoneum of uremic rats treated with PD demonstrated fibrosis, increased TGF-β expression, increased Smad2/3 activation, decreased Smad7 expression, and increased expression of fibrogenic and angiogenic factors. In addition, peritoneal function was impaired and its structure was altered, including a thickened submesothelial layer. In rats transfected with a Smad7 transgene using an ultrasound-microbubble-mediated system, peritoneal fibrosis was attenuated, peritoneal function was improved, and Smad2/3 activation was inhibited. We suggest that administration of Smad7 inhibits peritoneal fibrogenesis in uremic rats treated with PD by correcting the imbalance between downregulated Smad7 and activated Smad2/3. Blockade of the TGF-β/Smad signaling pathway may represent a novel therapeutic approach to prevent peritoneal fibrosis in patients treated with PD. Copyright © 2007 by the American Society of Nephrology.en_HK
dc.languageengen_US
dc.publisherAmerican Society of Nephrology. The Journal's web site is located at http://www.jasn.orgen_HK
dc.relation.ispartofJournal of the American Society of Nephrologyen_HK
dc.subject.meshAnimalsen_US
dc.subject.meshExtracellular Matrix - Metabolismen_US
dc.subject.meshFibrosis - Metabolismen_US
dc.subject.meshGene Expressionen_US
dc.subject.meshGene Therapyen_US
dc.subject.meshMaleen_US
dc.subject.meshNeovascularization, Pathologic - Metabolismen_US
dc.subject.meshPeritoneal Dialysis, Continuous Ambulatory - Adverse Effectsen_US
dc.subject.meshPeritoneal Diseases - Etiology - Metabolism - Therapyen_US
dc.subject.meshPeritoneum - Metabolism - Pathologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshSignal Transduction - Physiologyen_US
dc.subject.meshSmad7 Protein - Genetics - Metabolismen_US
dc.subject.meshTransfectionen_US
dc.subject.meshTransforming Growth Factor Beta - Metabolismen_US
dc.subject.meshTransgenesen_US
dc.subject.meshUremia - Metabolism - Therapyen_US
dc.titleSmad7 transgene attenuates peritoneal fibrosis in uremic rats treated with peritoneal dialysisen_HK
dc.typeArticleen_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.emailKar, NL: knlai@hku.hken_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.identifier.authorityKar, NL=rp00324en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1681/ASN.2007010121en_HK
dc.identifier.pmid17855642-
dc.identifier.scopuseid_2-s2.0-34948897937en_HK
dc.identifier.hkuros147906-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34948897937&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume18en_HK
dc.identifier.issue10en_HK
dc.identifier.spage2689en_HK
dc.identifier.epage2703en_HK
dc.identifier.isiWOS:000250985900012-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridGuo, H=55468645700en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridMan, FL=11640357700en_HK
dc.identifier.scopusauthoridChan, LYY=55182644100en_HK
dc.identifier.scopusauthoridTsang, AWL=7006979244en_HK
dc.identifier.scopusauthoridHui, YL=7103107517en_HK
dc.identifier.scopusauthoridKar, NL=7402135706en_HK
dc.identifier.citeulike1811199-
dc.customcontrol.immutablejt 130530-

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