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• W4386823867 abstract "Abstract Background Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by synovial inflammation, causing substantial disability and reducing life quality. While macrophages are widely appreciated as a master regulator in the inflammatory response of RA, the precise mechanisms underlying the regulation of proliferation and inflammation in RA-derived fibroblast-like synoviocytes (RA-FLS) remain elusive. Here, we provide extensive evidence to demonstrate that macrophage contributes to RA microenvironment remodeling by extracellular vesicles (sEVs) and downstream miR-100-5p/ mammalian target of rapamycin (mTOR) axis. Results We showed that cBMDM-sEVs exhibited a notable increase in abundance compared with nBMDM-sEVs. cBMDM-sEVs induced significant RA-FLS proliferation and potent inflammatory responses. Mechanistically, decreased levels of miR-100-5p were detected in cBMDM-sEVs compared with nBMDM-sEVs. miR-100-5p overexpression ameliorated RA-FLS proliferation and inflammation by targeting the mTOR pathway. Partial attenuation of the inflammatory effects induced by cBMDM-sEVs on RA-FLS was achieved through the introduction of an overexpression of miR-100-5p. Conclusions Our work reveals the critical role of macrophages in exacerbating RA by facilitating the transfer of miR-100-5p-deficient sEVs to RA-FLS, and sheds light on novel disease mechanisms and provides potential therapeutic targets for RA interventions." @default.
• W4386823867 created "2023-09-19" @default.
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• W4386823867 date "2023-09-18" @default.
• W4386823867 modified "2023-10-01" @default.
• W4386823867 title "Macrophage-Derived miR-100-5p Orchestrates Synovial Proliferation and Inflammation in Rheumatoid Arthritis through mTOR Signaling" @default.
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• W4386823867 doi "https://doi.org/10.21203/rs.3.rs-3329888/v1" @default.
• W4386823867 hasPublicationYear "2023" @default.
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