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Article: Rapamycin-induced modulation of miRNA expression is associated with amelioration of HIV-associated nephropathy (HIVAN)

TitleRapamycin-induced modulation of miRNA expression is associated with amelioration of HIV-associated nephropathy (HIVAN)
Authors
KeywordsApoptosis
Epithelial mesanchymal transition
HIV-associated nephropathy
Mammalian target of rapamycin
MicroRNA
Issue Date2013
Citation
Experimental Cell Research, 2013, v. 319 n. 13, p. 2073-2080 How to Cite?
AbstractRecent studies suggested that miRNAs are involved in the development of the pathogenesis of HIV-associated nephropathy (HIVAN). Rapamycin, a widely used mTOR inhibitor, has been demonstrated to slow down the progression of HIVAN. However, the role of miRNA in the regulation of these processes has not been investigated so far. In the current study, we have used a microarray-based approach in combination with real-time PCR to profile the miRNA expression patterns in rapamycin-treated HIVAN mice (Tg26). Our results demonstrated that 19 miRNAs belonging to 13 different families expressed differentially in renal tissues of rapamycin-receiving Tg26 mice when compared to Tg26 mice-receiving saline only. The patterns of miRNAs expression in rapamycin-receiving Tg26 mice took a reverse turn. These miRNAs were classified into 8 functional categories. In in vitro studies, we examined the expression of specific miRNAs in HIV-1 transduced human podocytes (HIV/HPs). HIV/HPs displayed attenuation of expression of miR-99a, -100a, -199a and miR-200, whereas, rapamycin inhibited this effect of HIV. These findings suggest that rapamycin-mediated up-regulation of specific miRNAs could contribute to amelioration of renal lesions in HIVAN mice. © 2013 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/195407
ISSN
2023 Impact Factor: 3.3
2023 SCImago Journal Rankings: 0.947
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorCheng, K-
dc.contributor.authorRai, P-
dc.contributor.authorPlagov, A-
dc.contributor.authorLan, X-
dc.contributor.authorMathieson, PW-
dc.contributor.authorSaleem, MA-
dc.contributor.authorHusain, M-
dc.contributor.authorMalhotra, A-
dc.contributor.authorSinghal, PC-
dc.date.accessioned2014-02-28T06:12:06Z-
dc.date.available2014-02-28T06:12:06Z-
dc.date.issued2013-
dc.identifier.citationExperimental Cell Research, 2013, v. 319 n. 13, p. 2073-2080-
dc.identifier.issn0014-4827-
dc.identifier.urihttp://hdl.handle.net/10722/195407-
dc.description.abstractRecent studies suggested that miRNAs are involved in the development of the pathogenesis of HIV-associated nephropathy (HIVAN). Rapamycin, a widely used mTOR inhibitor, has been demonstrated to slow down the progression of HIVAN. However, the role of miRNA in the regulation of these processes has not been investigated so far. In the current study, we have used a microarray-based approach in combination with real-time PCR to profile the miRNA expression patterns in rapamycin-treated HIVAN mice (Tg26). Our results demonstrated that 19 miRNAs belonging to 13 different families expressed differentially in renal tissues of rapamycin-receiving Tg26 mice when compared to Tg26 mice-receiving saline only. The patterns of miRNAs expression in rapamycin-receiving Tg26 mice took a reverse turn. These miRNAs were classified into 8 functional categories. In in vitro studies, we examined the expression of specific miRNAs in HIV-1 transduced human podocytes (HIV/HPs). HIV/HPs displayed attenuation of expression of miR-99a, -100a, -199a and miR-200, whereas, rapamycin inhibited this effect of HIV. These findings suggest that rapamycin-mediated up-regulation of specific miRNAs could contribute to amelioration of renal lesions in HIVAN mice. © 2013 Elsevier Inc.-
dc.languageeng-
dc.relation.ispartofExperimental Cell Research-
dc.subjectApoptosis-
dc.subjectEpithelial mesanchymal transition-
dc.subjectHIV-associated nephropathy-
dc.subjectMammalian target of rapamycin-
dc.subjectMicroRNA-
dc.titleRapamycin-induced modulation of miRNA expression is associated with amelioration of HIV-associated nephropathy (HIVAN)-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.yexcr.2013.04.011-
dc.identifier.pmid23611955-
dc.identifier.scopuseid_2-s2.0-84879884921-
dc.identifier.volume319-
dc.identifier.issue13-
dc.identifier.spage2073-
dc.identifier.epage2080-
dc.identifier.isiWOS:000322055800015-
dc.identifier.issnl0014-4827-

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