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http://purl.uniprot.org/citations/35678923http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/35678923http://www.w3.org/2000/01/rdf-schema#comment"

Background

Circular RNA (circRNA) is widely shown to be associated with the development of diabetic nephropathy (DN). Our study aimed to further explore the role of circ_0000064 and provide a new mechanism for its action in DN.

Methods

Cell models of DN in vitro were constructed by treating human renal mesangial cells (HRMCs) with high glucose (HG). The expression of circ_0000064, microRNA-424-5p (miR-424-5p) and Wnt family member 2B (WNT2B) mRNA was detected by quantitative real-time PCR (qPCR). Cell proliferation was assessed by CCK-8 assay and EdU assay. Cell cycle was characterized by DNA content using flow cytometry. The releases of pro-inflammatory factors were checked using commercial ELISA kits. The expression of cell cycle- and fibrosis-associated proteins was detected by western blot. The interplays between miR-424-5p and circ_0000064 or WNT2B were verified by dual-luciferase reporter assay and RIP assay.

Results

Circ_0000064 and WNT2B were upregulated, while miR-424-5p was downregulated in HG-treated HRMCs. Circ_0000064 knockdown largely attenuated HG-induced proliferation, inflammatory responses and extracellular matrix (ECM) accumulation in HRMCs, and miR-424-5p deficiency reversed the role of circ_0000064 knockdown. MiR-424-5p was a target of circ_0000064, and miR-424-5p directly bound to WNT2B. MiR-424-5p restoration alleviated HG-induced proliferation, inflammatory responses and ECM accumulation in HRMCs, and WNT2B overexpression partially abolished the effects of miR-424-5p.

Conclusion

Circ_0000064 knockdown ameliorated HG-induced HRMC dysfunctions through miR-424-5p enrichment-mediated WNT2B inhibition, hinting that circ_0000064 contributed to DN development."xsd:string
http://purl.uniprot.org/citations/35678923http://purl.org/dc/terms/identifier"doi:10.1007/s10157-022-02241-w"xsd:string
http://purl.uniprot.org/citations/35678923http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/35678923http://purl.uniprot.org/core/author"Zhao Q."xsd:string
http://purl.uniprot.org/citations/35678923http://purl.uniprot.org/core/author"Min Y."xsd:string
http://purl.uniprot.org/citations/35678923http://purl.uniprot.org/core/date"2022"xsd:gYear
http://purl.uniprot.org/citations/35678923http://purl.uniprot.org/core/name"Clin Exp Nephrol"xsd:string
http://purl.uniprot.org/citations/35678923http://purl.uniprot.org/core/pages"943-954"xsd:string
http://purl.uniprot.org/citations/35678923http://purl.uniprot.org/core/title"Circ_0000064 knockdown attenuates high glucose-induced proliferation, inflammation and extracellular matrix deposition of mesangial cells through miR-424-5p-mediated WNT2B inhibition in cell models of diabetic nephropathy."xsd:string
http://purl.uniprot.org/citations/35678923http://purl.uniprot.org/core/volume"26"xsd:string
http://purl.uniprot.org/citations/35678923http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/35678923
http://purl.uniprot.org/citations/35678923http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/35678923
http://purl.uniprot.org/uniprot/#_Q5TEH8-mappedCitation-35678923http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/35678923
http://purl.uniprot.org/uniprot/#_Q93097-mappedCitation-35678923http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/35678923
http://purl.uniprot.org/uniprot/Q93097http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/35678923
http://purl.uniprot.org/uniprot/Q5TEH8http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/35678923