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白细胞介素-17A加剧大鼠颈动脉内氯化铁诱导的动脉血栓形成。

Interleukin-17A Exacerbates Ferric Chloride-Induced Arterial Thrombosis in Rat Carotid Artery.

作者信息

Maione Francesco, Parisi Antonio, Caiazzo Elisabetta, Morello Silvana, D'Acquisto Fulvio, Mascolo Nicola, Cicala Carla

机构信息

Department of Pharmacy, University of Naples Federico II, Via Domenico Montesano 49, 80131 Naples, Italy.

Department of Pharmaceutical and Biomedical Sciences, University of Salerno, Via Ponte Don Melillo, Fisciano, 84084 Salerno, Italy.

出版信息

Int J Inflam. 2014;2014:247503. doi: 10.1155/2014/247503. Epub 2014 Apr 3.

DOI:10.1155/2014/247503
PMID:24940514
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3997091/
Abstract

Interleukin-17A (IL-17A), the most widely studied member of the IL-17 cytokine family, is a cytokine which emerged to be critical for host defense as well as in the pathogenesis of autoimmune disorders. Moreover, IL-17A is involved in the pathogenesis of cardiovascular diseases, such as atherosclerosis and acute coronary syndrome and in the cardiovascular risk associated with systemic immunological disorders. Consistent with this, we have recently shown that IL-17A increases human and murine platelet response to ADP. In this study we expanded our previous observation and we describe for the first time an in vivo prothrombotic effect of the cytokine. Our results show that IL-17A is synergic with a low FeCl3 concentration in inducing carotid thrombus in rats and suggest that the effect is likely related to a downregulation of CD39 vascular expression and hydrolyzing activity. Our findings indicate that IL-17A might be an important molecule at the interface between hemostasis and inflammation. "This paper is dedicated to the memory of Professor Alfredo Colonna"

摘要

白细胞介素-17A(IL-17A)是白细胞介素-17细胞因子家族中研究最广泛的成员,是一种对宿主防御以及自身免疫性疾病发病机制至关重要的细胞因子。此外,IL-17A还参与心血管疾病的发病机制,如动脉粥样硬化和急性冠状动脉综合征,以及与全身性免疫疾病相关的心血管风险。与此一致的是,我们最近发现IL-17A会增强人和小鼠血小板对ADP的反应。在本研究中,我们扩展了之前的观察结果,并首次描述了该细胞因子在体内的促血栓形成作用。我们的结果表明,IL-17A与低浓度FeCl3协同作用可诱导大鼠颈动脉血栓形成,提示该作用可能与CD39血管表达及水解活性下调有关。我们的研究结果表明,IL-17A可能是止血与炎症之间界面上的一个重要分子。“本文谨献给阿尔弗雷多·科隆纳教授”

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/838d/3997091/baf5ce13db05/IJI2014-247503.004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/838d/3997091/4622fa2bd6cc/IJI2014-247503.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/838d/3997091/aa693bf9a11e/IJI2014-247503.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/838d/3997091/baf5ce13db05/IJI2014-247503.004.jpg

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Transgenic over expression of ectonucleotide triphosphate diphosphohydrolase-1 protects against murine myocardial ischemic injury.
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