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Article: MicroRNA-29b inhibits diabetic nephropathy in db/db mice

TitleMicroRNA-29b inhibits diabetic nephropathy in db/db mice
Authors
Issue Date2014
Citation
Molecular Therapy, 2014, v. 22, n. 4, p. 842-853 How to Cite?
AbstractInflammation and its consequent fibrosis are two main features of diabetic nephropathy (DN), but target therapy on these processes for DN remains yet ineffective. We report here that miR-29b is a novel therapeutic agent capable of inhibiting progressive renal inflammation and fibrosis in type 2 diabetes in db/db mice. Under diabetic conditions, miR-29b was largely downregulated in response to advanced glycation end (AGE) product, which was associated with upregulation of collagen matrix in mesangial cells via the transforming growth factor-β (TGF-β)/Smad3-dependent mechanism. These pathological changes were reversed by overexpressing miR-29b, but enhanced by knocking-down miR-29b. Similarly, loss of renal miR-29b was associated with progressive diabetic kidney injury, including microalbuminuria, renal fibrosis, and inflammation. Restored renal miR-29b by the ultrasound-based gene therapy was capable of attenuating diabetic kidney disease. Further studies revealed that inhibition of Sp1 expression, TGF-β/Smad3-dependent renal fibrosis, NF-κB-driven renal inflammation, and T-bet/Th1-mediated immune response may be mechanisms associated with miR-29b treatment in db/db mice. In conclusion, miR-29b may play a protective role in diabetic kidney disease and may have therapeutic potential for diabetic kidney complication. © The American Society of Gene & Cell Therapy.
Persistent Identifierhttp://hdl.handle.net/10722/199942
ISSN
2015 Impact Factor: 6.938
2015 SCImago Journal Rankings: 3.374
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorChen, Hai-Yong-
dc.contributor.authorZhong, Xiang-
dc.contributor.authorHuang, Xiaoru-
dc.contributor.authorMeng, Xiaoming-
dc.contributor.authorYou, Yongke-
dc.contributor.authorChung, Arthurck-
dc.contributor.authorLan, Huiyao-
dc.date.accessioned2014-07-26T23:10:56Z-
dc.date.available2014-07-26T23:10:56Z-
dc.date.issued2014-
dc.identifier.citationMolecular Therapy, 2014, v. 22, n. 4, p. 842-853-
dc.identifier.issn1525-0016-
dc.identifier.urihttp://hdl.handle.net/10722/199942-
dc.description.abstractInflammation and its consequent fibrosis are two main features of diabetic nephropathy (DN), but target therapy on these processes for DN remains yet ineffective. We report here that miR-29b is a novel therapeutic agent capable of inhibiting progressive renal inflammation and fibrosis in type 2 diabetes in db/db mice. Under diabetic conditions, miR-29b was largely downregulated in response to advanced glycation end (AGE) product, which was associated with upregulation of collagen matrix in mesangial cells via the transforming growth factor-β (TGF-β)/Smad3-dependent mechanism. These pathological changes were reversed by overexpressing miR-29b, but enhanced by knocking-down miR-29b. Similarly, loss of renal miR-29b was associated with progressive diabetic kidney injury, including microalbuminuria, renal fibrosis, and inflammation. Restored renal miR-29b by the ultrasound-based gene therapy was capable of attenuating diabetic kidney disease. Further studies revealed that inhibition of Sp1 expression, TGF-β/Smad3-dependent renal fibrosis, NF-κB-driven renal inflammation, and T-bet/Th1-mediated immune response may be mechanisms associated with miR-29b treatment in db/db mice. In conclusion, miR-29b may play a protective role in diabetic kidney disease and may have therapeutic potential for diabetic kidney complication. © The American Society of Gene & Cell Therapy.-
dc.languageeng-
dc.relation.ispartofMolecular Therapy-
dc.titleMicroRNA-29b inhibits diabetic nephropathy in db/db mice-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/mt.2013.235-
dc.identifier.pmid24445937-
dc.identifier.pmcidPMC3982502-
dc.identifier.scopuseid_2-s2.0-84897577501-
dc.identifier.hkuros232084-
dc.identifier.volume22-
dc.identifier.issue4-
dc.identifier.spage842-
dc.identifier.epage853-
dc.identifier.eissn1525-0024-

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