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首页> 外文期刊>Cytokine >ADMA induces monocyte adhesion via activation of chemokine receptors in cultured THP-1 cells.
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ADMA induces monocyte adhesion via activation of chemokine receptors in cultured THP-1 cells.

机译：ADMA通过激活培养的THP-1细胞中的趋化因子受体诱导单核细胞粘附。

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摘要

Asymmetric dimethylarginine (ADMA), an endogenous NOS inhibitor, is also an important inflammatory factor contributing to the development of atherosclerosis (AS). The present study was to test the effect of ADMA on angiotensin (Ang) II-induced monocytic adhesion. Human monocytoid cells (THP-1) or isolated peripheral blood monocyte cells (PBMCs) were incubated with Ang II (10(-6)M) or exogenous ADMA (30 microM) for 4 or 24h in the absence or presence of losartan or antioxidant PDTC. In cultured THP-1 cells, Ang II (10(-6)M) for 24h elevated the level of ADMA in the medium, upregulated the protein expression of protein arginine methyltransferase (PRMT) and decreased the activity of dimethylarginine dimethylaminohydrolase (DDAH). Both of Ang II and ADMA increased monocytic adhesion to human umbilical vein endothelial cells (HUVECs), elevated the levels of monocyte chemoattractant protein (MCP)-1, interleukin (IL)-8 and tumor necrosis factor (TNF)-alpha and upregulated CCR(2) and CXCR(2) mRNA expression, concomitantly with increase in reactive oxygen species (ROS) generation and activation of nuclear factor (NF)-kappaB. Pretreatment with losartan (10 microM) or PDTC (10 microM) abolished the effects mediated by Ang II or ADMA. In isolated PBMCs from healthy individuals, ADMA upregulated the expression of CXCR(2) mRNA, which was attenuated by losartan (10 microM), however, ADMA had no effect on surface protein expression of CCR(2). The present results suggest that ADMA may be involved in monocytic adhesion induced by Ang II via activation of chemokine receptors by ROS/NF-kappaB pathway.
机译：内源性NOS抑制剂非对称二甲基精氨酸（ADMA）也是促成动脉粥样硬化（AS）发展的重要炎症因子。本研究旨在测试ADMA对血管紧张素（Ang）II诱导的单核细胞粘附的影响。在不存在或存在氯沙坦或抗氧化剂的情况下，将人单核细胞（THP-1）或分离的外周血单核细胞（PBMC）与Ang II（10（-6）M）或外源性ADMA（30 microM）孵育4或24h PDTC。在培养的THP-1细胞中，Ang II（10（-6）M）持续24h可提高培养基中ADMA的水平，上调蛋白精氨酸甲基转移酶（PRMT）的蛋白表达，并降低二甲基精氨酸二甲基氨基水解酶（DDAH）的活性。 Ang II和ADMA均增加了单核细胞对人脐静脉内皮细胞（HUVEC）的粘附，单核细胞趋化蛋白（MCP）-1，白介素（IL）-8和肿瘤坏死因子（TNF）-α的水平升高以及CCR上调（2）和CXCR（2）mRNA表达，同时伴随活性氧（ROS）生成和核因子（NF）-kappaB激活的增加。用氯沙坦（10 microM）或PDTC（10 microM）进行的预处理消除了由Ang II或ADMA介导的作用。在来自健康个体的分离的PBMC中，ADMA上调了CXCR（2）mRNA的表达，氯沙坦（10 microM）减弱了该表达，但是，ADMA对CCR（2）的表面蛋白表达没有影响。目前的结果表明，ADMA可能通过ROS /NF-κB途径激活趋化因子受体而参与Ang II诱导的单核细胞粘附。

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