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PubMed · 10733939

CD39 modulates IL-1 release from activated endothelial cells.

M Imai·C Goepfert·E Kaczmarek·S C Robson
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Abstract

The activation of endothelial cells (EC) and monocyte-macrophages (Mφ) by lipopolysaccharide (LPS) is considered an important element of the vascular injury observed in endotoxemia. Interleukin-1 (IL-1) beta release from Mφ 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-1alpha release. Overexpression of CD39 following infection with recombinant CD39 adenoviral vectors (AdCD39) abrogated the initial phase of ATP secretion and inhibited IL-1alpha release; comparable results were obtained with soluble NTPDase. These data demonstrate that CD39/NTPDase modulates IL-1alpha release from LPS stimulated human EC.

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Adenosine TriphosphatasesAdenosine TriphosphateAntigens, CDApyraseEndothelium, VascularEndotoxemiaHumansInterleukin-1LipopolysaccharidesRecombinant ProteinsJournal ArticleResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.

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M Imai, C Goepfert, E Kaczmarek, S C Robson. 2000-04-02. CD39 modulates IL-1 release from activated endothelial cells.. https://doi.org/10.1006/bbrc.2000.2410

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