ArticleImmunity, inflammation and disease2025
PLSCR1 Regulates the Physiology of Fibroblast-Like Synoviocytes via Modulating the STAT1 Signaling Pathway.
Article in Immunity, inflammation and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundRheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation and joint destruction. Elucidating the molecular mechanisms underlying the pathogenesis is crucial for identifying novel therapeutic targets. Phospholipid scramblase 1 (PLSCR1) has been implicated in systemic autoimmune diseases. However, the function and underlying mechanism in RA remains unclear.
methodsReverse transcriptase-quantitative polymerase chain reaction was used to detect the expression levels of PLSCR1 in the serum of 30 RA patients and 30 healthy controls. The function of PLSCR1 in human fibroblast-like synoviocytes (HFLSs) was investigated by siRNA-mediated knockdown. Cell proliferation, apoptosis, and inflammatory cytokine production were assessed through 5-ethynyl-2'-deoxyuridine (EdU) assays, flow cytometry and enzyme-linked immunosorbent assays. The regulatory relationship between PLSCR1 and signal transducer and activator of transcription 1 (STAT1) was further explored using 2-NP rescue experiments.
resultsPLSCR1 was significantly upregulated in the serum of RA patients. Silencing PLSCR1 in HFLSs led to decreased proliferation, increased apoptosis, reduced levels of tumor necrosis factor alpha, interleukin-1-beta, and IL-6, and downregulation of STAT1 expression. Notably, activation of STAT1 signaling reversed the effects of PLSCR1 knockdown, restoring proliferative capacity and inflammatory cytokine production while reducing apoptosis.
conclusionPLSCR1 is upregulated in RA and regulates the proliferation, apoptosis and inflammation of FLSs by modulating the STAT1 signaling pathway. These findings suggest that PLSCR1 may serve as a potential molecular target for RA therapy.
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