File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

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
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
2015 Impact Factor: 3.378
2015 SCImago Journal Rankings: 1.900
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.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-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats