<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Xu W</submitter><funding>Yantai Science and Technology Bureau</funding><funding>Key Technology Research and Development Program of Shandong</funding><funding>Medical and Health Science and Technology Development Project of Shandong Province</funding><pagination>14545-14561</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9995129</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(6)</volume><pubmed_abstract>Rheumatoid arthritis (RA) is a most common chronic joint disease belonging to inflammatory autoimmune disease. The aim of this study was to determine the role and mechanism of bone marrow mesenchymal stem cells (BMSCs)-derived exosomes and fibrinogen-like protein 1 (FGL1) overexpression exosomes shuttled by BMSCs (FGL1-Exos) on RA. All of the exosomes were visualized by transmission electron microscope (TEM) and the characteristic proteins were detected by western blot. To investigate the therapeutic effect of FGL1-Exos, RA-FLSs were activated by TNF-α and RA rat model was established by collagen incomplete Freund's adjuvant. Cell viability, apoptosis, inflammation factors, and protein levels were detected by CCK-8, flow cytometry, enzyme-linked immunosorbent assay and western blot, respectively. Hematoxylin and eosin and safranin O staining were used to detect the histopathology changes. Cell apoptosis and FGL1 expression in knee joint were detected by immunofluorescence. The results showed that FGL1-Exos could inhibit the cell viability meanwhile increase the cell apoptosis in RA-FLSs. Meanwhile, FGL1-Exos could effectively suppress the inflammation score, joint destruction, and inflammatory response in RA rat model. FGL1-Exos directly inhibited cell apoptosis of RA-FLSs and RA rat model by suppressing the inflammatory cytokines, specific rheumatoid markers, immunological markers meanwhile meditating the NF-κB pathway. Our results indicate that FGL1 was a therapeutic potential target in RA therapy.</pubmed_abstract><journal>Bioengineered</journal><pubmed_title>Exosomes derived from fibrinogen-like protein 1-overexpressing bone marrow-derived mesenchymal stem cells ameliorates rheumatoid arthritis.</pubmed_title><pmcid>PMC9995129</pmcid><funding_grant_id>2016WS0696</funding_grant_id><funding_grant_id>2016WS033</funding_grant_id><funding_grant_id>2016GSF201112</funding_grant_id><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Li W</pubmed_authors><pubmed_authors>Wang X</pubmed_authors><pubmed_authors>Xu W</pubmed_authors><pubmed_authors>Qu W</pubmed_authors><pubmed_authors>Su H</pubmed_authors><pubmed_authors>Cheng Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Exosomes derived from fibrinogen-like protein 1-overexpressing bone marrow-derived mesenchymal stem cells ameliorates rheumatoid arthritis.</name><description>Rheumatoid arthritis (RA) is a most common chronic joint disease belonging to inflammatory autoimmune disease. The aim of this study was to determine the role and mechanism of bone marrow mesenchymal stem cells (BMSCs)-derived exosomes and fibrinogen-like protein 1 (FGL1) overexpression exosomes shuttled by BMSCs (FGL1-Exos) on RA. All of the exosomes were visualized by transmission electron microscope (TEM) and the characteristic proteins were detected by western blot. To investigate the therapeutic effect of FGL1-Exos, RA-FLSs were activated by TNF-α and RA rat model was established by collagen incomplete Freund's adjuvant. Cell viability, apoptosis, inflammation factors, and protein levels were detected by CCK-8, flow cytometry, enzyme-linked immunosorbent assay and western blot, respectively. Hematoxylin and eosin and safranin O staining were used to detect the histopathology changes. Cell apoptosis and FGL1 expression in knee joint were detected by immunofluorescence. The results showed that FGL1-Exos could inhibit the cell viability meanwhile increase the cell apoptosis in RA-FLSs. Meanwhile, FGL1-Exos could effectively suppress the inflammation score, joint destruction, and inflammatory response in RA rat model. FGL1-Exos directly inhibited cell apoptosis of RA-FLSs and RA rat model by suppressing the inflammatory cytokines, specific rheumatoid markers, immunological markers meanwhile meditating the NF-κB pathway. Our results indicate that FGL1 was a therapeutic potential target in RA therapy.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jun</publication><modification>2025-04-18T14:02:08.904Z</modification><creation>2025-04-04T14:46:59.006Z</creation></dates><accession>S-EPMC9995129</accession><cross_references><pubmed>36694465</pubmed><doi>10.1080/21655979.2022.2090379</doi></cross_references></HashMap>