ArticleArthritis research & therapy2021
Upregulated endonuclease Regnase-1 suppresses osteoarthritis by forming a negative feedback loop of catabolic signaling in chondrocytes.
Article in Arthritis research & therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- The regnase family in autoimmune diseases: a regnase-1-centered perspective on cellular heterogeneity.Molecular biology reports · 2026Review
- Tristetraprolin protects against osteoarthritis by restraining chondrocyte mitochondrial DNA release through post-transcriptional regulation.Journal of orthopaedic translation · 2026Article
- Roquin-1 interaction with Regnase-1 inhibits the progression of rheumatoid arthritis via suppressing FGF2 expression and NF-κB pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- In-vivo screening implicates endoribonuclease Regnase-1 in modulating senescence-associated lysosomal changes.GeroScience · 2024Article
- Osteoarthritis year in review: genetics, genomics, epigenetics.Osteoarthritis and cartilage · 2022Review
- Inhibitory Effects of IL-6-Mediated Matrix Metalloproteinase-3 and -13 byPharmaceuticals (Basel, Switzerland) · 2021Article
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Authors and funding
2 authors at 1 institution in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundRibonucleases (RNases) play central roles in the post-transcriptional regulation of mRNA stability. Our preliminary results revealed that the endonuclease Regnase-1 is specifically upregulated in osteoarthritic chondrocytes. We herein explored the possible functions and regulatory mechanisms of Regnase-1 in a mouse model of osteoarthritis (OA).
methodsThe expression and target genes of Regnase-1 were identified by microarray analysis in primary-culture mouse articular chondrocytes. Experimental OA in mice was induced by destabilization of the medial meniscus (DMM). The function of Regnase-1 in DMM-induced post-traumatic OA mice was examined by adenovirus-mediated overexpression or knockdown in knee joint tissues, and also by using Regnase-1 heterozygous knockout mice (Zc3h12a
resultsAmong the RNases, Regnase-1 was exclusively upregulated in chondrocytes stimulated with OA-associated catabolic factors. Adenovirus-mediated overexpression or knockdown of Regnase-1 alone in joint tissues did not cause OA-like changes. However, overexpression of Regnase-1 in joint tissues significantly ameliorated DMM-induced post-traumatic OA cartilage destruction, whereas knockdown or genetic ablation of Regnase-1 exacerbated DMM-induced cartilage destruction. Mechanistic studies suggested that Regnase-1 suppresses cartilage destruction by modulating the expression of matrix-degrading enzymes in chondrocytes.
conclusionOur results collectively suggest that upregulated Regnase-1 in OA chondrocytes may function as a chondro-protective effector molecule during OA pathogenesis by forming a negative feedback loop of catabolic signals, such as matrix-degrading enzyme expression, in OA chondrocytes.
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