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TL1A(TNFSF15)-ENO1 axis promotes osteoarthritis by disrupting redox homeostasis via the PI3K/AKT pathway[II]

ABSTRACT: Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by progressive cartilage degradation, chronic inflammation, and chondrocyte senescence. Tumor necrosis factor-like cytokine 1A (TL1A), a member of the TNF superfamily, has recently been implicated in regulating inflammatory processes and tissue remodeling. However, its precise role in OA pathogenesis remains incompletely understood. In this study, we investigated the impact of TL1A deficiency on OA progression and its underlying mechanism with a focus on oxidative stress-induced chondrocyte senescence.

ORGANISM(S): Homo sapiens

PROVIDER: GSE286154 | GEO | 2025/02/01

REPOSITORIES: GEO

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TL1A deficiency attenuates osteoarthritis by regulating oxidative stress-induced senescence in articular chondrocytes [I]

Project description:Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by progressive cartilage degradation, chronic inflammation, and chondrocyte senescence. Tumor necrosis factor-like cytokine 1A (TL1A), a member of the TNF superfamily, has recently been implicated in regulating inflammatory processes and tissue remodeling. However, its precise role in OA pathogenesis remains incompletely understood. In this study, we investigated the impact of TL1A deficiency on OA progression and its underlying mechanism with a focus on oxidative stress-induced chondrocyte senescence.

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TL1A(TNFSF15)-ENO1 axis promotes osteoarthritis by disrupting redox homeostasis via the PI3K/AKT pathway[II]

Project description:TL1A(TNFSF15)-ENO1 axis promotes osteoarthritis by disrupting redox homeostasis via the PI3K/AKT pathway[II]

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Expression data (U133 Plus 2.0) from fibroblast like synoviocytes from patients with rheumatoid arthritis (RA-FLS) stimulated by TL1A

Project description:TNF-like ligand 1A (TL1A) is a member of TNF receptor superfamily and involved in the pathogenesis of autoimmune diseases by inducing apoptosis via intracellular death domain or promoting inflammation through the activation of NFM-NM-:B by binding to its specific receptor death receptor 3 (DR3). Meanwhile, decoy receptor 3 (DcR3) competitively binds soluble TL1A in addition to Fas-ligand (FasL) and LIGHT and inhibits the signaling of TL1A via DR3. DcR3 overexpressed in rheumatoid synovial fibroblasts (RA-FLS) stimulated with inflammatory cytokines such as TNFM-NM-1 or IL-1M-NM-2 inhibits Fas-induced apoptosis. In contrast, DcR3 inhibited cell proliferation induced by inflammatory cytokines via membrane-bound TL1A expressed on RA-FLS. Therefore, TL1A-DcR3/DR3 signaling may be involved in the pathogenesis of RA by modulating apoptosis and proliferation of RA-FLS. We hypothesized that TL1A regulates the gene expression in RA-FLS. We used to search for genes in which expression in RA-FLS is regulated by the ligation of TL1A. RA-FLS were obtained from 4 RA patients (sample1-4). Each sample was incubated with either 1.0 M-NM-<g/ml recombinant human TL1A protein or phosphate buffered saline (PBS) diluted with serum-free Opti-MEM medium as non-stimulated control for 12 hours at 37M-BM-0C with 5% CO2. Gene expression in RA-FLS stimulated by TL1A was compared with that of their respective non-stimulated controls.

2014-12-10 | E-GEOD-63995 | biostudies-arrayexpress

Expression data (U133 Plus 2.0) from fibroblast like synoviocytes from patients with rheumatoid arthritis (RA-FLS) stimulated by TL1A

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The long noncoding RNA ELDR serves as an epigenetic driver in aging and injury-induced chondrocyte senescence [lncRNA]

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Expression data (U133 Plus 2.0) from fibroblast like synoviocytes from patients with rheumatoid arthritis (RA-FLS) stimulated by TL1A

Project description:TNF-like ligand 1A (TL1A) is a member of TNF receptor superfamily and involved in the pathogenesis of autoimmune diseases by inducing apoptosis via intracellular death domain or promoting inflammation through the activation of NFκB by binding to its specific receptor death receptor 3 (DR3). Meanwhile, decoy receptor 3 (DcR3) competitively binds soluble TL1A in addition to Fas-ligand (FasL) and LIGHT and inhibits the signaling of TL1A via DR3. DcR3 overexpressed in rheumatoid synovial fibroblasts (RA-FLS) stimulated with inflammatory cytokines such as TNFα or IL-1β inhibits Fas-induced apoptosis. In contrast, DcR3 inhibited cell proliferation induced by inflammatory cytokines via membrane-bound TL1A expressed on RA-FLS. Therefore, TL1A-DcR3/DR3 signaling may be involved in the pathogenesis of RA by modulating apoptosis and proliferation of RA-FLS. We hypothesized that TL1A regulates the gene expression in RA-FLS. We used to search for genes in which expression in RA-FLS is regulated by the ligation of TL1A.

2014-12-10 | GSE63995 | GEO

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