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http://purl.uniprot.org/citations/32931797http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/32931797http://www.w3.org/2000/01/rdf-schema#comment"

Aims

Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been reported as the important regulators in osteoarthritis (OA). However, the detailed mechanism is implicated. The aim of this study is to reveal the functional mechanism of lncRNA ARFRP1 and miR-15a-5p in osteoarthritis.

Materials and methods

The expression level of genes was detected by quantitative real time polymerase chain reaction (qRT-PCR) or western blot assay. Cell Counting Kit-8 (CCK-8) was used to assess cell viability. Cell apoptosis rate was analyzed by flow cytometry analysis. Furthermore, Enzyme-linked immunosorbent assay (ELISA) was performed to measure tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-1β contents. The interaction between miR-15a-5p and ARFRP1 or Toll-like receptor 4 (TLR4) was predicted by miRcode or PITA, and then confirmed by the dual luciferase reporter assay or pull down assay. Besides, NF-κB-driven luciferase activity was determined using NF-κB luciferase reporter assay.

Key findings

ARFRP1 and TLR4 levels were increased and miR-15a-5p level was decreased in OA cartilage tissues and lipopolysaccharides (LPS)-induced chondrocytes. ARFRP1 knockdown inhibited LPS-induced the injury of chondrocytes. Interestingly, miR-15a-5p downregulated by ARFRP1 negatively modulated TLR4 expression through interaction. ARFRP1 mediated LPS-induced the injury of chondrocytes via regulating miR-15a-5p/TLR4 axis. Furthermore, ARFRP1 exerted function by modulation of NF-κB pathway.

Significance

Our findings confirmed that ARFRP1 mediated LPS-induced the injury of chondrocytes through regulating NF-κB pathway by modulation of miR-15a-5p/TLR4 axis, providing theoretical basis for the treatment of OA patients."xsd:string
http://purl.uniprot.org/citations/32931797http://purl.org/dc/terms/identifier"doi:10.1016/j.lfs.2020.118429"xsd:string
http://purl.uniprot.org/citations/32931797http://purl.uniprot.org/core/author"Zhang Q."xsd:string
http://purl.uniprot.org/citations/32931797http://purl.uniprot.org/core/author"Zhang G."xsd:string
http://purl.uniprot.org/citations/32931797http://purl.uniprot.org/core/author"Zhu J."xsd:string
http://purl.uniprot.org/citations/32931797http://purl.uniprot.org/core/author"Tang J."xsd:string
http://purl.uniprot.org/citations/32931797http://purl.uniprot.org/core/author"Nie M."xsd:string
http://purl.uniprot.org/citations/32931797http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/32931797http://purl.uniprot.org/core/name"Life Sci"xsd:string
http://purl.uniprot.org/citations/32931797http://purl.uniprot.org/core/pages"118429"xsd:string
http://purl.uniprot.org/citations/32931797http://purl.uniprot.org/core/title"LncRNA ARFRP1 knockdown inhibits LPS-induced the injury of chondrocytes by regulation of NF-kappaB pathway through modulating miR-15a-5p/TLR4 axis."xsd:string
http://purl.uniprot.org/citations/32931797http://purl.uniprot.org/core/volume"261"xsd:string
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