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- W2589681871 abstract "Mesenchymal stem cells (MSCs) undergo premature senescence when challenged with oxidative and metabolic stresses. Pro-inflammatory cytokines were reported to activate or damage MSCs. It is unclear whether cytokines provoke the cellular changes via premature senescence. To determine whether cytokines induce premature senescence, we treated bone marrow-derived MSCs (BM-MSC) with IL-1β, TNFα or vehicle for up to 48h. Cell growth, p16 and p21 expressions, senescence-associated β-galactosidase (SA-βGal) as well as cell morphology were analyzed. Neither IL-1β nor TNFα induced growth arrest or expression of p16 or p21. Cell morphology was not overtly altered when compared with control cells. By contrast, SA-βgal was increased by IL-1β and TNFα. Since SA-βgal increase was reported to be due to expansion of lysosome mass, we analyzed lysosomes by Lysotracker staining. Lysotracker staining was enhanced in cells treated with TNFα or IL-1β. TNFα and IL-1β induced autophagy as evidenced by increased LC3-II on western ..." @default.
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- W2589681871 date "2016-04-01" @default.
- W2589681871 modified "2023-09-22" @default.
- W2589681871 title "Pro-inflammatory cytokines induce mesenchymal stem cell secretory phenotype by increasing autophagosomes and lysosomes" @default.
- W2589681871 doi "https://doi.org/10.1096/fasebj.30.1_supplement.1062.2" @default.
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