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DC Field | Value | Language |
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dc.contributor.author | Ricardo S.D. | en |
dc.contributor.author | Wang B. | en |
dc.contributor.author | Yao K. | en |
dc.contributor.author | Wise A.F. | en |
dc.contributor.author | Lau R. | en |
dc.contributor.author | Shen H.-H. | en |
dc.contributor.author | Tesch G.H. | en |
dc.date.accessioned | 2021-05-14T13:28:16Z | en |
dc.date.available | 2021-05-14T13:28:16Z | en |
dc.date.copyright | 2017 | en |
dc.date.created | 20170323 | en |
dc.date.issued | 2017-03-23 | en |
dc.identifier.citation | Clinical Science. 131 (5) (pp 411-423), 2017. Date of Publication: 2017. | en |
dc.identifier.issn | 0143-5221 | en |
dc.identifier.uri | https://repository.monashhealth.org/monashhealthjspui/handle/1/39470 | en |
dc.description.abstract | The regulatory role of a novel miRNA, miR-378, was determined in the development of fibrosis through repression of the MAPK1 pathway, miR-378 and fibrotic gene expression was examined in streptozotocin (STZ)-induced diabetic mice at 18 weeks or in unilateral ureteral obstruction (UUO) mice at 7 days. miR-378 transfection of proximal tubular epithelial cells, NRK52E and mesangial cells was assessed with/without endogenous miR-378 knockdown using the locked nucleic acid (LNA) inhibitor. NRK52E cells were co-transfected with the mothers against decapentaplegic homolog 3 (SMAD3) CAGA reporter and miR-378 in the presence of transforming growth factor-beta (TGF-beta1) was assessed. Quantitative polymerase chain reaction (qPCR) showed a significant reduction in miR-378 (P < 0.05) corresponding with up-regulated type I collagen, type IV collagen and a-smooth muscle actin (SMA) in kidneys of STZ or UUO mice, compared with controls. TGF-beta1 significantly increased mRNA expression of type I collagen (P < 0.05), type IV collagen (P < 0.05) and alpha-SMA (P < 0.05) in NRK52E cells, which was significantly reduced (P < 0.05) following miR-378 transfection and reversed following addition of the LNA inhibitor of endogenous miR-378. Overexpression of miR-378 inhibited mesangial cell expansion and proliferation in response to TGF-beta1, with LNA-miR-378 transfection reversing this protective effect, associated with cell morphological alterations. The protective function of MAPK1 on miR-378 was shown in kidney cells treated with the MAPK1 inhibitor, selumetinib, which inhibited mesangial cell hypertrophy in response to TGF-beta1. Taken together, these results suggest that miR-378 acts via regulation of the MAPK1 pathway. These studies demonstrate the protective function of MAPK1, regulated by miR-378, in the induction of kidney cell fibrosis and mesangial hypertrophy.Copyright © 2017 The Author(s). | en |
dc.language | en | en |
dc.language | English | en |
dc.publisher | Portland Press Ltd | en |
dc.relation.ispartof | Clinical Science | en |
dc.title | miR-378 reduces mesangial hypertrophy and kidney tubular fibrosis via MAPK signalling. | en |
dc.type | Article | en |
dc.identifier.affiliation | Nephrology | en |
dc.identifier.doi | http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1042/CS20160571 | en |
dc.publisher.place | United Kingdom | en |
dc.identifier.pubmedid | 28053239 [http://www.ncbi.nlm.nih.gov/pubmed/?term=28053239] | en |
dc.identifier.source | 614815530 | en |
dc.identifier.institution | (Wang, Yao, Wise, Lau, Ricardo) Department of Anatomy and Developmental Biology, Biomedicine Discovery Institute, Monash University, Clayton, Australia (Shen) Department of Materials Engineering, Monash University, Clayton, Australia (Tesch) Department of Nephrology, Monash University Department of Medicine, Monash Medical Centre, Clayton, VIC, Australia | en |
dc.description.address | S.D. Ricardo, Department of Anatomy and Developmental Biology, Biomedicine Discovery Institute, Monash University, Clayton, Australia. E-mail: sharon.ricardo@monash.edu | en |
dc.description.publicationstatus | Embase | en |
dc.rights.statement | Copyright 2017 Elsevier B.V., All rights reserved. | en |
dc.identifier.authoremail | Ricardo S.D.; sharon.ricardo@monash.edu | en |
dc.identifier.affiliationext | (Wang, Yao, Wise, Lau, Ricardo) Department of Anatomy and Developmental Biology, Biomedicine Discovery Institute, Monash University, Clayton, Australia | - |
dc.identifier.affiliationext | (Shen) Department of Materials Engineering, Monash University, Clayton, Australia | - |
dc.identifier.affiliationmh | (Tesch) Department of Nephrology, Monash University Department of Medicine, Monash Medical Centre, Clayton, VIC, Australia | - |
item.cerifentitytype | Publications | - |
item.fulltext | No Fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.grantfulltext | none | - |
item.openairetype | Article | - |
Appears in Collections: | Articles |
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