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http://purl.uniprot.org/citations/31066587http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31066587http://www.w3.org/2000/01/rdf-schema#comment"

Background

Understanding the mechanism of chondrocytes degeneration could provide a new potential therapeutic idea for rheumatoid arthritis (RA) treatment. MicroRNA-27b-3p (miR-27b-3p) has been shown to regulate a variety of cell behaviors in various cell types. However, the role of miR-27b-3p in RA remains unknown.

Materials and methods

Expression of miR-27b-3p and HIPK2 in cartilage tissues and chondrocytes was characterized using qRT-PCR and Western blot. MiR-27b-3p was overexpressed or suppressed in chondrocytes to observe the potential role of miR-27b-3p.

Results

We found declined miR-27b-3p and elevated HIPK2 in RA tissues and cells using qRT-PCR. Dual-luciferase reporter assay validated HIPK2 is a direct target of miR-27b-3p, confirmed by Western blot results. Pearson correlation presented that there was a significantly negative correlation between miR-27b-3p and HIPK2 mRNA. Overexpression of miR-27b-3p significantly reduced the expression of pro-apoptotic protein c-caspase3 and increased the expression of anti-apoptotic Bcl-2; however, downregulation of miR-27b-3p has a significant effect of inducing apoptosis. Furthermore, overexpression of miR-27b-3p combined with recombinant HIPK2 protein showed the inhibitory effect of miR-27b-3p was abolished by HIPK2.

Conclusion

We found declined miR-27b-3p and elevated HIPK2 in RA tissues and cells. Further in vitro studies demonstrated that miR-27b might inhibit chondrocyte apoptosis and thus attenuate RA development by directly inhibiting HIPK2 expression."xsd:string
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http://purl.uniprot.org/citations/31066587http://purl.uniprot.org/core/author"Chen P."xsd:string
http://purl.uniprot.org/citations/31066587http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/31066587http://purl.uniprot.org/core/author"Li S."xsd:string
http://purl.uniprot.org/citations/31066587http://purl.uniprot.org/core/author"Liu R."xsd:string
http://purl.uniprot.org/citations/31066587http://purl.uniprot.org/core/author"Yang J."xsd:string
http://purl.uniprot.org/citations/31066587http://purl.uniprot.org/core/author"Zhou Y."xsd:string
http://purl.uniprot.org/citations/31066587http://purl.uniprot.org/core/author"Xia D."xsd:string
http://purl.uniprot.org/citations/31066587http://purl.uniprot.org/core/author"Yang B."xsd:string
http://purl.uniprot.org/citations/31066587http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/31066587http://purl.uniprot.org/core/name"Artif Cells Nanomed Biotechnol"xsd:string
http://purl.uniprot.org/citations/31066587http://purl.uniprot.org/core/pages"1766-1771"xsd:string
http://purl.uniprot.org/citations/31066587http://purl.uniprot.org/core/title"MicroRNA-27b-3p inhibits apoptosis of chondrocyte in rheumatoid arthritis by targeting HIPK2."xsd:string
http://purl.uniprot.org/citations/31066587http://purl.uniprot.org/core/volume"47"xsd:string
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