کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2019525 | 1542219 | 2013 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Sphingosine-1-phosphate receptor-2 mediated NFκB activation contributes to tumor necrosis factor-α induced VCAM-1 and ICAM-1 expression in endothelial cells
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کلمات کلیدی
TNFαICAM-1HUVECGPCRS1PSphKVCAM-1ECs - EC هاG-protein coupled receptor - G-پروتئین همراه گیرندهsphingolipids - اسفنگولیپیدSphingosine kinase - اسپینوزین کینازSphingosine-1-phosphate - اسپینگسین-1-فسفاتtumor necrosis factor-α - تومور نکروز عامل αHuman umbilical vein endothelial cells - سلول های اندوتلیالی ورید ناف انسانVasculature - مجاورIntercellular adhesion molecule 1 - مولکول چسبندگی بین سلولی 1Vascular cell adhesion molecule 1 - مولکول چسبندگی سلولی عروقی 1
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Sphingosine-1-phosphate (S1P) regulates a wide array of biological functions in endothelial cells. We previously showed that S1P receptor subtype 2 (S1P2) is significantly up-regulated in the atherosclerotic endothelium (J. Biol. Chem. 283:30363, 2008). In this study, we investigated the roles of S1P2-mediated signaling in the proinflammatory responses of endothelial cells. Treatment with tumor necrosis factor-α (TNFα), a proinflammatory cytokine, increased the expression of S1P2 receptors in endothelial cells. TNFα treatment also enhanced sphingosine kinase 1 expression and increased S1P production. Pharmacological inhibition or knockdown of S1P2 receptors completely abrogated the TNFα-induced VCAM-1 (vascular cell adhesion molecule 1) and ICAM-1 (intercellular adhesion molecule 1) expression in endothelial cells. In contrast, pharmacological inhibition or knockdown of other S1P receptor subtypes had no effect on the TNFα-stimulated ICAM-1 and VCAM-1 expression. Moreover, ectopic expression of S1P2 receptors increased VCAM-1 and ICAM-1 expression in endothelial cells in response to S1P stimulation. Mechanistically, we show that antagonizing S1P2 signaling markedly inhibited the TNFα-stimulated NFκB activation. Utilizing the NFκB reporter luciferase assay, the S1P/S1P2 signaling was shown to stimulate NFκB activation. Moreover, the S1P/S1P2-stimulated VCAM-1/ICAM-1 expression was completely abolished by the pharmacological inhibitor of NFκB. Collectively, our data suggest that TNFα treatment activates autocrine S1P/S1P2 signaling, which subsequently activates NFκB and leads to the proinflammatory responses in endothelial cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Prostaglandins & Other Lipid Mediators - Volume 106, October 2013, Pages 62-71
Journal: Prostaglandins & Other Lipid Mediators - Volume 106, October 2013, Pages 62-71
نویسندگان
Wenliang Zhang, Jin An, Hiba Jawadi, Deanna L. Siow, Jen-Fu Lee, Jiawei Zhao, Allison Gartung, Krishna Rao Maddipati, Kenneth V. Honn, Binks W. Wattenberg, Menq-Jer Lee,