ArticleArthritis research & therapy2024
Investigation of GPM6B as a novel therapeutic target in Osteoarthritis.
Article in Arthritis research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Macrophages: pivotal orchestrators and emerging therapeutic targets in osteoarthritis pathogenesis.Journal of translational medicine · 2025Review
- Ultrasonography as an Early Evaluation Tool for Posttraumatic Osteoarthritis in Wistar Rats (Rattus norvegicus).Journal of the American Association for Laboratory Animal Science : JAALAS · 2025Article
- Article
- Glycoprotein M6B suppresses the maintenance of glioma stem cell stemness and proliferation via the integrin β1/β-catenin pathway.Frontiers in molecular biosciences · 2025Article
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Authors and funding
7 authors.
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Abstract
backgroundOsteoarthritis (OA) is the most common motor system disease in older people, characterized by a high incidence and significant social and economic burden. Women have a higher risk of OA, more severe clinical symptoms, and a higher rate of disabilities than men. However, the pathogenesis of OA remains unclear. Therefore, we screened for differentially expressed genes (DEGs) in OA patients of different sex and searched for new targets that may be involved in regulating the development of OA.
methodsThe study compared the expression of DEGs in synovial fluid exosomes between male and female patients with OA through RNA sequencing combined with bioinformatics analysis using public data. To evaluate the screened DEGs, synovial tissue and fluid samples were obtained from patients with OA who underwent joint replacement surgery. SiRNA-mediated knockdown in vitro experiments were performed to investigate the role of glycoprotein membrane 6B (GPM6B). Meanwhile, GPM6B gene knockout mice were used to assess the in vivo pathological roles of GPM6B in OA.
resultsThe results revealed that GPM6B is a potential target associated with OA. Immunofluorescence staining demonstrated that GPM6B was expressed in fibroblast-like synoviocytes (FLS) and macrophage-like synoviocytes in patients with OA. In vitro experiments confirmed that GPM6B knockdown can reduce the expression of inflammatory factors in primary FLS from patients with OA. Under inflammatory conditions, GPM6B knockdown can reduce the expression of matrix metalloproteinases as well as proliferation of FLS. In addition, using a destabilization of the medial meniscus-induced OA model, we revealed that GPM6B is associated with OA progression in mice.
conclusionThus, we provided evidence that GPM6B act as a new target associated with OA.
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