ArticleJournal of orthopaedic surgery and research2021
Recombinant TSG-6 protein inhibits the growth of capsule fibroblasts in frozen shoulder via suppressing the TGF-β/Smad2 signal pathway.
Article in Journal of orthopaedic surgery and research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- Immune Cell Causality and Glucocorticoid Trade-Off in Frozen Shoulder: Integrative MR-RNA-Seq Analysis.Biomedicines · 2026Article
- Identification of an immediate-early gene-activated fibroblast state in frozen shoulder capsular fibrosis.iScience · 2026Article
- Hyperlipidemia exacerbates frozen shoulder fibrosis by activating the TGF-β/Smad2/3 signaling pathway via the TBX5-TNC-Itgα2 axis.iScience · 2026Article
- Signaling pathway networks in frozen shoulder fibrosis: from inflammatory initiation to fibrotic progression.Frontiers in medicine · 2026Review
- From inflammatory activation to fibrotic remodeling: the central role of macrophage heterogeneity in frozen shoulder.Frontiers in immunology · 2026Review
- Frozen shoulder: a narrative review of current treatment concepts and the underlying scientific evidence.Clinics in shoulder and elbow · 2025Article
- Temporal dynamics of ADSC therapy in skin fibrosis: unraveling the roles of ROS/NF-κB/TSG-6 signaling axis.Stem cell research & therapy · 2025Article
- Basic Science Research in Frozen Shoulder: Current Updates.Indian journal of orthopaedics · 2025Article
- Identification and validation of biomarkers, construction of diagnostic models, and investigation of immunological infiltration characteristics for idiopathic frozen shoulder.Frontiers in immunology · 2025Article
- MAP3K19 Promotes the Progression of Tuberculosis-Induced Pulmonary Fibrosis Through Activation of the TGF-β/Smad2 Signaling Pathway.Molecular biotechnology · 2024Article
- TGF-β1 induces formation of TSG-6-enriched extracellular vesicles in fibroblasts which can prevent myofibroblast transformation by modulating Erk1/2 phosphorylation.Scientific reports · 2024Article
- Role of TGF-β and p38 MAPK in TSG-6 Expression in Adipose Tissue-Derived Stem Cells In Vitro and In Vivo.International journal of molecular sciences · 2023Article
- Cytokines' Role in the Pathogenesis and Their Targeting for the Prevention of Frozen Shoulder: A Narrative Review.Cureus · 2023Review
- Antifibrotic TSG-6 Expression Is Synergistically Increased in Both Cells during Coculture of Mesenchymal Stem Cells and Macrophages via the JAK/STAT Signaling Pathway.International journal of molecular sciences · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe tumor necrosis factor-stimulated gene-6 (TSG-6) has been confirmed to inhibit inflammation. It is now generally accepted that local inflammatory stimulation around shoulder capsule causes proliferative fibrosis. This study aims to investigate the mechanism of recombinant TSG-6 protein inhibiting the growth of capsule fibroblasts in frozen shoulder via the TGF-β/Smad2 signal pathway.
methodsHuman frozen shoulder capsule tissue was taken for primary and passage culture, and the 3rd generation fibroblasts from pathological frozen shoulder capsule were treated with different concentrations of recombinant TSG-6 protein, or with TGF-β1 agonist SRI-011381. Immunoconfocal analysis was used to identify the isolated fibroblasts, and MTT assay, colony formation assay, and flow cytometry were used to detect the viability, proliferation, and apoptosis rate of fibroblast. The contents of fibrosis and inflammation indexes COL1A1, TNF-α, IL-6, and IL-1β in the cell supernatant were detected using ELISA and then further examined by qRT-PCR. The expression of Bax, Bcl-2, and proteins related to TGF-β/Smad2 pathway were detected by Western Blot.
resultsCompared with the blank control group, fibroblasts intervened with TSG-6 (2 μg and 5 μg) showed significantly decreased viability and proliferation ability and enhanced cell apoptosis, concurrent with the reductions in Bcl-2 expression; COL1A1, TNF-α, IL-6, and IL-1β levels; and the expression of TGF-β1 and phosphorylated Smad22, and an increase in Bax expression, while SRI-011381 treatment would reverse the effect of recombinant TSG-6 protein.
conclusionRecombinant TSG-6 protein inhibited the growth of primary fibroblasts from human frozen shoulder capsule by suppressing the TGF-β/Smad2 signaling pathway.
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