The pathogenesis of rheumatoid arthritis (RA) is heavily impacted by the inflammation and activation of fibroblast-like synoviocytes (FLS). The objective of this investigation is to clarify the involvement of exosomes derived from FLS stimulated by tumour necrosis factor α (TNF-α) in angiogenesis and the underlying mechanisms. FLS cells were obtained from synovial fluid of RA patients and exosomes were obtained from FLS cell supernatant with TNF-α stimulation by ultracentrifugation.
View Article and Find Full Text PDFObjective: This retrospective analysis was to assess the role of Janus kinases (JAK) inhibitors compared with conventional disease modifying anti-rheumatic drugs (DMRADs) in the treatment of polymyalgia rheumatica (PMR) with glucocorticoids (GCs) reduction.
Methods: Clinical information was collected from PMR patients in the JAK inhibitor group and the DMARDs group from January 2020 to August 2021 at Jiaxing first Hospital. Serum C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), hemoglobin (Hb), albumin and dose of GCs before and after treatment were compared between two groups.
Connect Tissue Res
November 2022
Objective: To clarify the role of glucocerebrosidase (GBA) and Ceramide (Cer) in rheumatoid arthritis (RA).
Methods: GBA-expressing lentivirus were constructed and injected into collagen-induced arthritis (CIA) mice, and compared with CIA mice injected with empty vector. The severity of arthritis and inflammatory mediators were evaluated.
Objectives: SLE is a chronic autoimmune disease, which can affect the level of bone metabolism and increase the risk of osteoporosis and fracture. The purpose of this research is to study the effect of SLE on bone turnover markers without the influence of glucocorticoids.
Methods: A total of 865 female subjects were recruited from Zhejiang Provincial People's Hospital and the First Hospital of Jiaxing, including 391 SLE patients without the influence of glucocorticoids and 474 non-SLE people.
High mobility group box protein 1 (HMGB1) plays an important role in the pathogenesis of rheumatoid arthritis (RA), but the pathogenic mechanisms of HMGB1 in RA and the involvement of the lysosomal enzyme acid β-glucosidase 1 (GBA1) are not fully elucidated. The aim of the present study was to use HMGB1 to treat RA synovial fibroblasts (RASFs) and to examine the changes of transcriptional factors. RASFs were isolated from synovial tissues obtained from five RA patients undergoing synovectomy or joint replacement.
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