ArticleArthritis & rheumatology (Hoboken, N.J.)2019
Genetic Inactivation of ZCCHC6 Suppresses Interleukin-6 Expression and Reduces the Severity of Experimental Osteoarthritis in Mice.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 31 citations in OpenAlex.
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- An update on the use of conventional and biological disease-modifying anti-rheumatic drugs in hand osteoarthritis.Therapeutic advances in musculoskeletal disease · 2023Review
- Synovial inflammation in osteoarthritis progression.Nature reviews. Rheumatology · 2022Review
- DNA Methylation and Detoxification in the EarthwormToxics · 2022Article
- ERK1/2-mediated activation of DRP1 regulates mitochondrial dynamics and apoptosis in chondrocytes.Osteoarthritis and cartilage · 2022Article
- Exome Sequencing of 5 Families with Severe Early-Onset Periodontitis.Journal of dental research · 2022Article
- Identification of Key Genes and Pathways in Osteoarthritis via Bioinformatic Tools: An Updated Analysis.Cartilage · 2021Article
- The distinct roles of zinc finger CCHC-type (ZCCHC) superfamily proteins in the regulation of RNA metabolism.RNA biology · 2021Review
- A retrotransposon gag-like-3 gene RTL3 and SOX-9 co-regulate the expression of COL2A1 in chondrocytes.Connective tissue research · 2021Article
- Terminal uridyltransferase 7 regulates TLR4-triggered inflammation by controlling Regnase-1 mRNA uridylation and degradation.Nature communications · 2021Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveCytokine expression is tightly regulated posttranscriptionally, but high levels of interleukin-6 (IL-6) in patients with osteoarthritis (OA) indicate that regulatory mechanisms are disrupted in this disorder. The enzyme ZCCHC6 (zinc-finger CCHC domain-containing protein 6; TUT-7) has been implicated in posttranscriptional regulation of inflammatory cytokine expression, but its role in OA pathogenesis is unknown. The present study was undertaken to investigate whether ZCCHC6 directs the expression of IL-6 and influences OA pathogenesis in vivo.
methodsHuman and mouse chondrocytes were stimulated with recombinant IL-1β. Expression of ZCCHC6 in human chondrocytes was knocked down using small interfering RNAs. IL-6 transcript stability was determined by actinomycin D chase, and 3'-uridylation of microRNAs was determined by deep sequencing. Zcchc6
resultsZCCHC6 was markedly up-regulated in damaged cartilage from human OA patients and from wild-type mice with surgically induced OA. Overexpression of ZCCHC6 induced the expression of IL-6, and its knockdown reduced IL-6 transcript stability and IL-1β-induced IL-6 expression in chondrocytes. Reintroduction of Zcchc6 in Zcchc6
conclusionThese findings indicate that ZCCHC6 enhances IL-6 expression in chondrocytes through transcript stabilization and by uridylating miR-26b, which abrogates repression of IL-6. Inhibition of IL-6 expression and significantly reduced OA severity in Zcchc6
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