File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
  • Find via Find It@HKUL
Supplementary

Conference Paper: Inhibition of miR-34a reduces podocyte apoptosis by targeting Bcl-2 and autophagy

TitleInhibition of miR-34a reduces podocyte apoptosis by targeting Bcl-2 and autophagy
Authors
Issue Date2015
PublisherAmerican Society of Nephrology. The Journal's web site is located at http://www.jasn.org
Citation
The 2015 Annual Meeting of the American Society of Nephrology (ASN) - Kidney Week 2015, San Diego CA., 3-8 November 2015. In Journal of the American Society of Nephrology, 2015, v. 26 abstract suppl., p. 953A, abstract no. PUB286 How to Cite?
AbstractBACKGROUND: Podocyte apoptosis is a key event in the pathogenesis of diabetic nephropathy. MiR-34a has been reported to be involved in cell proliferation and apoptosis, but its potential roles in podocytes under the diabetic condition remains unknown. METHODS: Type 2 diabetic nephropathy was established by uninephrectomy (Unx) in nine-week-old db/db mice. In cultured immortalized human podocytes, miR-34a was overexpressed or knocked down by transfection with miR-34a precursor (pre-34a) or inhibitor (anti-34a), respectively. Podocytes were exposed to glycated human serum albumin (AGEs) and then examined for the expression of apoptosis and autophagy markers. The expression of miR-34a in mouse renal cortex and cultured podocytes were determined by quantitative PCR (Q-PCR) using specific Taqman miRNA assay. RESULTS: Compared with control group, Unx db/db mice(n=7) showed significantly higher expression level of miR-34a in renal cortex. In cultured human podocytes, exposure to AGEs also markedly increased miR-34a expression. The anti-apoptosis genes Bcl-2 and survivin, podocyte cytoskeleton molecule synaptopodin, tight junction protein ZO-1, as well as autophagy marker LC3-II, were all reduced after AGE treatment. Moreover, inhibition of miR-34a by transfection with anti-34a in podocytes prevented AGE-induced apoptosis by rescue of Bcl-2 and LC3-II expression. CONCLUSIONS: Our data demonstrated that miR-34a is involved in podocyte injury under diabetic conditions. Inhibition of miR-34a in podocytes attenuates apoptosis induced by AGEs via enhancing expression of Bcl-2 and regulating autophagy. These results indicate that targeting miR-34a might be a potential therapeutic strategy for diabetic nephropathy. This study is supported by the National Basic Research Program of China 973 program no. 2012CB517600 (no. 2012CB517606), Small Project Funding (project code 201309176123)
Persistent Identifierhttp://hdl.handle.net/10722/232435
ISSN
2015 Impact Factor: 8.491
2015 SCImago Journal Rankings: 4.699

 

DC FieldValueLanguage
dc.contributor.authorLiu, Y-
dc.contributor.authorLi, R-
dc.contributor.authorYiu, WH-
dc.contributor.authorWu, H-
dc.contributor.authorWong, WLD-
dc.contributor.authorLeung, JCK-
dc.contributor.authorChan, LY-
dc.contributor.authorLai, KN-
dc.contributor.authorSaleem, M-
dc.contributor.authorMathieson, PW-
dc.contributor.authorTang, SCW-
dc.date.accessioned2016-09-20T05:29:57Z-
dc.date.available2016-09-20T05:29:57Z-
dc.date.issued2015-
dc.identifier.citationThe 2015 Annual Meeting of the American Society of Nephrology (ASN) - Kidney Week 2015, San Diego CA., 3-8 November 2015. In Journal of the American Society of Nephrology, 2015, v. 26 abstract suppl., p. 953A, abstract no. PUB286-
dc.identifier.issn1046-6673-
dc.identifier.urihttp://hdl.handle.net/10722/232435-
dc.description.abstractBACKGROUND: Podocyte apoptosis is a key event in the pathogenesis of diabetic nephropathy. MiR-34a has been reported to be involved in cell proliferation and apoptosis, but its potential roles in podocytes under the diabetic condition remains unknown. METHODS: Type 2 diabetic nephropathy was established by uninephrectomy (Unx) in nine-week-old db/db mice. In cultured immortalized human podocytes, miR-34a was overexpressed or knocked down by transfection with miR-34a precursor (pre-34a) or inhibitor (anti-34a), respectively. Podocytes were exposed to glycated human serum albumin (AGEs) and then examined for the expression of apoptosis and autophagy markers. The expression of miR-34a in mouse renal cortex and cultured podocytes were determined by quantitative PCR (Q-PCR) using specific Taqman miRNA assay. RESULTS: Compared with control group, Unx db/db mice(n=7) showed significantly higher expression level of miR-34a in renal cortex. In cultured human podocytes, exposure to AGEs also markedly increased miR-34a expression. The anti-apoptosis genes Bcl-2 and survivin, podocyte cytoskeleton molecule synaptopodin, tight junction protein ZO-1, as well as autophagy marker LC3-II, were all reduced after AGE treatment. Moreover, inhibition of miR-34a by transfection with anti-34a in podocytes prevented AGE-induced apoptosis by rescue of Bcl-2 and LC3-II expression. CONCLUSIONS: Our data demonstrated that miR-34a is involved in podocyte injury under diabetic conditions. Inhibition of miR-34a in podocytes attenuates apoptosis induced by AGEs via enhancing expression of Bcl-2 and regulating autophagy. These results indicate that targeting miR-34a might be a potential therapeutic strategy for diabetic nephropathy. This study is supported by the National Basic Research Program of China 973 program no. 2012CB517600 (no. 2012CB517606), Small Project Funding (project code 201309176123)-
dc.languageeng-
dc.publisherAmerican Society of Nephrology. The Journal's web site is located at http://www.jasn.org-
dc.relation.ispartofJournal of the American Society of Nephrology-
dc.titleInhibition of miR-34a reduces podocyte apoptosis by targeting Bcl-2 and autophagy-
dc.typeConference_Paper-
dc.identifier.emailLiu, Y: liuyang9@hku.hk-
dc.identifier.emailYiu, WH: whyiu@hku.hk-
dc.identifier.emailLeung, JCK: jckleung@hku.hk-
dc.identifier.emailLai, KN: knlai@hku.hk-
dc.identifier.emailMathieson, PW: president@hku.hk-
dc.identifier.emailTang, SCW: scwtang@hku.hk-
dc.identifier.authorityLeung, JCK=rp00448-
dc.identifier.authorityLai, KN=rp00324-
dc.identifier.authorityMathieson, PW=rp01885-
dc.identifier.authorityTang, SCW=rp00480-
dc.identifier.hkuros265352-
dc.identifier.volume26-
dc.identifier.issueabstract suppl.-
dc.identifier.spage953A, abstract no. PUB286-
dc.identifier.epage953A, abstract no. PUB286-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats