國家衛生研究院 NHRI:Item 3990099045/10780
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    題名: Pro-inflammatory cytokines induce mesenchymal stem cell secretory phenotype by increasing autophagosomes and lysosomes
    作者: Hsueh, YC;Chen, HL;Chang, TC;Wu, KKY
    貢獻者: Institute of Cellular and Systems Medicine
    摘要: 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 blotting and LC3 immunofluorescence staining. Co-localization analysis revealed increased auto-lysosomes. However, LC3-positive autophagosomes exceeded lysosomes. TNFα and IL-1β-induced autophagosomes were correlated with increased expression of cyclooxygenase-2, prostaglandin E synthase, IL-6, IL-8 and TSG-6. Work is in progress to determine whether inhibition of lysosomes and/or autophagosomes influences cytokine expression. Our findings indicate that TNFα and IL-1β induces BM-MSC secretory phenotype without accompanied cell senescence through activating autophagy and increasing autolysosomes.
    日期: 2016-04
    關聯: The FASEB Journal. 2016 Apr;30(1, Suppl.):Meeting Abstract 1062.2.
    Link to: http://www.fasebj.org/content/30/1_Supplement/1062.2.abstract?sid=690de247-3097-4785-a8aa-d46f19f57807
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0892-6638&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000406444001488
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