國家衛生研究院 NHRI:Item 3990099045/10796
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    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.nhri.org.tw/handle/3990099045/10796


    题名: Cytokine-induced autophagy promotes long-term VCAM-1 but not ICAM-1 expression by degrading late-phase Ikappa Balpha
    其它题名: Cytokine-induced autophagy promotes long-term VCAM-1 but not ICAM-1 expression by degrading late-phase IκBα
    作者: Chu, LY;Hsueh, YC;Cheng, HL;Wu, KK
    贡献者: Institute of Cellular and Systems Medicine
    摘要: Pro-inflammatory cytokines are known to induce endothelial cell autophagy, but the role of autophagy in regulating the expression of pro-inflammatory molecules has not been characterized. We hypothesized that autophagy facilitates expression of endothelial adhesion molecules. TNF alpha and IL-1 beta induced autophagy markers in human umbilical vein endothelial cells and inhibition of autophagy by 3-methyladenine (3-MA) blocked adhesion of Jurkat lymphocytes. Interestingly, 3-MA suppressed VCAM-1 but not ICAM-1 expression at 24 hours but not 6 hours. 3-MA suppressed VCAM-1 transcription and decreased nuclear NF-kappa B p65 level at 6 hours but not at 2 hours. Cytokines induced a biphasic degradation of I kappa B alpha and 3-MA selectively blocked the late-phase I kappa B alpha degradation. Our results suggest that cytokine-induced autophagy contributes to late-phase I kappa B alpha degradation, facilitates NF-kappa B nuclear translocation and VCAM-1 transcription for long-term VCAM-1 expression. With a cytokines array assay, we found that 3-MA also inhibited IP-10 expression. These findings provide new information about the role of endothelial autophagy in persistent expression of VCAM-1 and IP-10 which enhance lymphocyte recruitment and adhesion to endothelium.
    日期: 2017-09
    關聯: Scientific Reports. 2017 Sep;7:Article number 12472.
    Link to: http://dx.doi.org/10.1038/s41598-017-12641-8
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=2045-2322&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000412032600038
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