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Death-associated protein kinase 1 correlates with podocyte apoptosis and renal damage and can be mediated by miR-361

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dc.contributor.authorWu, Guang-jun
dc.contributor.authorZhao, Hong-biao
dc.contributor.authorZhang, Xiao-wei
dc.date.accessioned2023-01-31T12:01:55Z
dc.date.available2023-01-31T12:01:55Z
dc.date.issued2021
dc.description.abstractBackground. Herein, we aimed to determine whether DAPK1 and its post-transcriptional regulator miR-361 were implicated in high glucose (HG)-induced podocyte injury and renal damage in db/db mice. Materials and methods. Podocytes were incubated with normal glucose (NG; 5 mM) or HG (30 mM). Podocyte apoptosis was evaluated using TUNEL staining. Lentiviral-delivered specific short hairpin RNA (shRNA) was designed to silence DAPK1 expression in podocytes. miR-361 agomir was administrated by tail intravenous injection in db/db diabetic mice to investigate the renoprotection of miR-361 in vivo. Results. Exposure of podocytes to HG led to a significant increase in DAPK1 mRNA and protein levels and a decrease in miR-361 expression levels. Knockdown of DAPK1 attenuated HG-triggered growth inhibition, apoptosis, DNA damage and cell membrane damage in podocytes. Mechanically, DAPK1 was a direct target of miR-361. Transfection with miR-361 mimics into podocytes resulted in a significant decrease in the DAPK1 protein expression level. In addition, HGinduced the up-regulation of the DAPK1 protein expression level in podocytes was restrained by miR-361 mimics transfection. Intriguingly, overexpression of DAPK1 in HG-stimulated podocytes muted miR-361- mediated cytoprotection, including anti-apoptosis, resistance to DNA and membrane damage. In vivo, overexpression of miR-361 protected against hyperglycemia-induced podocyte loss, tubular atrophy and interstitial fibrosis in the kidney of db/db mice. Moreover, overexpression of miR-361 inhibited the protein expression of DAPK1 in the kidney of db/db mice. Conclusion. Our research presented a novel mechanism of HG-induced podocyte damage or renal lesion, supporting the miR-361/DAPK1 signaling pathway that could be used as a potential therapeutic target for the treatment of DN.es
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dc.format.extent13es
dc.identifier.citationHistology and Histopathology Vol. 36, nº11 (2021)
dc.identifier.doihttps://doi.org/10.14670/HH-18-358
dc.identifier.issn0213-3911
dc.identifier.issn1699-5848
dc.identifier.urihttp://hdl.handle.net/10201/127986
dc.languageenges
dc.publisherUniversidad de Murcia, Departamento de Biologia Celular e Histiologiaes
dc.relationSin financiación externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectmiR-361es
dc.subjectDAPK1es
dc.subjectPodocytees
dc.subjectHigh glucosees
dc.subjectApoptosises
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncologíaes
dc.titleDeath-associated protein kinase 1 correlates with podocyte apoptosis and renal damage and can be mediated by miR-361es
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.36,nº11 (2021)