Hypoxia/reoxygenation-induced HMGB1 translocation and release promotes islet proinflammatory cytokine production and early islet graft failure through TLRs signaling

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• 作者：Yao Cheng^a ; ^b ; ¹ ; Junjie Xiong^c ; ¹ ; Quan Chen^a ; ¹ ; Jie Xia^d ; ¹ ; Yi Zhang^c ; Xiaoyan Yang^a ; Kun Tao^a ; Shuang Zhang^a ; Sirong He ; MD ; PhD^a ; ^{hesirong@cqmu.edu.cn}
• 关键词：Intra-islet graft inflammation ; Hypoxia/reoxygenation ; High mobility group box 1 ; Toll-like receptors
• 刊名：Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：1863
• 期：2
• 页码：354-364
• 全文大小：2265 K
• 卷排序：1863

文摘

H/R up-regulation TLR2/4 and TLRs-mediated signaling, induces islets inflammatory. H/R-induced HMGB1 translocation and release can lead to islets inflammation. HMGB1-induced IL-1β need to activate JAK/STAT and JNK/p38 pathways through TLR2 signaling. HMGB1-Induced TNF-α production of islets are TLR4/NF-kB signaling dependent. HMGB1 inhibition reduced H/R-induced islets inflammation and early islet graft failure.