CD39 modulates IL-1 release from activated endothelial cells
CD39 modulates IL-1 release from activated endothelial cells
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DOI：
10.1006/bbrc.2000.2410
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发表时间：
2000-04-02
影响因子：
3.1
通讯作者：
Robson, SC
中科院分区：
文献类型：
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作者：
Imai, M;Goepfert, C;Robson, SC
脂多糖（LPS）激活内皮细胞（EC）和单核-巨噬细胞（M phi）被认为是内毒素血症中观察到的血管损伤的重要因素。白细胞介素-1（IL-1）β从M phi释放响应于LPS，似乎是通过P2 X7受体活化的ATP的自分泌/旁分泌释放介导的。在EC中，类似的核苷酸介导的信号传导途径可能受到CD 39（血管核苷三磷酸二磷酸水解酶（NTPD酶; ENTPD I））高水平表达的影响。为了确定CD 39是否调节ATP介导的IL-1从EC的释放，我们用LPS刺激人EC并测量ATP分泌和IL-1释放的水平。LPS触发EC分泌ATP，随后很快释放IL-1 α。用重组CD 39腺病毒载体（AdCD 39）感染后，CD 39的过表达消除了ATP分泌的初始阶段，并抑制了IL-1 α的释放;用可溶性NTPD酶获得了类似的结果。这些数据表明，CD 39/NTPD酶调节从LPS刺激的人EC释放IL-1 α。(C)北京大学出版社.
The activation of endothelial cells (EC) and monocyte-macrophages (M phi) by Lipopolysaccharide (LPS) is considered an important element of the vascular injury observed in endotoxemia. Interleukin-1 (IL-1) beta release from M phi in response to LPS, appears to be mediated by the autocrine/paracrine release of ATP via P2X7 receptor activation. In EC, similar nucleotide-mediated signaling pathways may be influenced by high levels of expression of CD39, the vascular nucleoside triphosphate diphosphohydrolase (NTPDase; ENTPD I). To determine whether CD39 modulates ATP-mediated release of IL-1 from EC, we stimulated human EC with LPS and measured levels of ATP secretion and IL-1 release. LPS triggered ATP secretion from EC that was soon followed by IL-1 alpha release. Overexpression of CD39 following infection with recombinant CD39 adenoviral vectors (AdCD39) abrogated the initial phase of ATP secretion and inhibited IL-1 alpha release; comparable results were obtained with soluble NTPDase. These data demonstrate that CD39/NTPDase modulates IL-1 alpha release from LPS stimulated human EC. (C) 2000 Academic Press.