Please use this identifier to cite or link to this item: http://hdl.handle.net/123456789/4109
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dc.contributor.authorAl-Azab, M.-
dc.contributor.authorWalana, W.-
dc.contributor.authorWei, J.-
dc.contributor.authorLi, W.-
dc.contributor.authorTang, Y.-
dc.contributor.authorWei, X.-
dc.contributor.authorAlmoiliqy, M.-
dc.contributor.authorShopit, A.-
dc.contributor.authorAbbas, E. E.-
dc.contributor.authorAdlat, S.-
dc.contributor.authorAwsh, M.-
dc.contributor.authorLi, X.-
dc.contributor.authorWang, B.-
dc.date.accessioned2023-11-21T14:24:02Z-
dc.date.available2023-11-21T14:24:02Z-
dc.date.issued2021-
dc.identifier.issn2005-5447-
dc.identifier.urihttp://hdl.handle.net/123456789/4109-
dc.description.abstractBackground and Objectives: The immunomodulatory potential of mesenchymal stem cells (MSCs) can be regulated by a variety of molecules, especially cytokines. The inflammatory cytokine, TNF-like ligand 1A (TL1A), has been reported as an inflammation stimulator in-multiple autoimmune diseases. Here, we studied the effects of TL1A/TNF-receptor 2 (TNFR2) pathway on the therapeutic potency of bone marrow-derived MSCs (BMSCs). Methods and Results: BMSCs, fibroblast-like synoviocytes (FLSs), and H9 and jurkat human T lymphocytes were used in this study. BMSCs paracrine activities, differentiation, proliferation, and migration were investigated after stim ulation with TL1A, and intervened with anti-TNFR2. Additionally, the effects of TL1A on BMSCs therapeutic potency were evaluated by treating RA-FLSs, and H9 and jurkat T cells with TL1A-stimulated BMSCs conditioned medium (CM). Indian hedgehog (IHH) involvement was determined by gene silencing and treatment by recombinant IHH (rIHH). TL1A induced BMSCs stemness-related genes, COX-2, IL-6, IDO, TGF-β and HGF through TNFR2. Also, TL1A corrected biased differentiation and increased proliferation, and migration through TNFR2. Meanwhile, CM of TL1A-stimulated BMSCs decreased the inflammatory markers of RA-FLSs and T cells. Moreover, TL1A-stimulated BMSCs experienced IHH up-regulation coupled with NF-κB and STAT3 signaling up-regulation, while p53 and oxidative stress were down-regulated. Furthermore, treatment of BMSCs by rIHH increased their anti-inflammatory effects. More importantly, knockdown of IHH decreased the ability of TL1A-stimulated BMSCs to alleviating the inflammation in RA-FLSs and T cells. Conclusions: This study reports the effects of TL1A/TNFR2 pathway on the biological behaviors and therapeutic po tency of BMSCs through IHH. These findings could introduce novel procedures to increase the stemness of MSCs in cellular therapy.en_US
dc.language.isoenen_US
dc.publisherKorean Society for Stem Cell Researchen_US
dc.relation.ispartofseriesVol. 14;No. 1-
dc.subjectBone Marrow-Derived Mesenchymal Stem Cellsen_US
dc.subjectTumor Necrosis Factor-Like Ligand 1Aen_US
dc.subjectTNF-Receptor 2en_US
dc.subjectIndian Hedgehogen_US
dc.titleTL1A/TNFR2 AXIS ENHANCES IMMUNOREGULATORY EFFECTS OF BONE MARROW DERIVED MESENCHYMAL STEM CELL BY INDIAN HEDGEHOG SIGNALING PATHWAYen_US
dc.typeArticleen_US
Appears in Collections:School of Medicine and Health Sciences



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