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首页> 外文期刊>Journal of cellular biochemistry. >PTX3, a key component of innate immunity, is induced by SAA via FPRL1-mediated signaling in HAECs.
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PTX3, a key component of innate immunity, is induced by SAA via FPRL1-mediated signaling in HAECs.

机译：SATX通过FPRL1介导的HAEC中的SAA信号诱导了先天免疫的关键成分PTX3。

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摘要

Serum amyloid A (SAA) is regarded as an important acute phase protein in coronary artery diseases. However, its involvement in the immune response of atherosclerosis is poorly understood. The present study was designed to investigate the influence of SAA on the secretion of long pentraxin 3 (PTX3), a key component of innate immunity, in human aortic endothelial cells (HAECs). Our study revealed that recombinant SAA up-regulated PTX3 production in a remarkable dose- and time-dependent manner and the activation of formyl peptide receptor-like 1 (FPRL1) was crucial for SAA-induced expression of PTX3 in HAECs. Meanwhile, SAA-induced PTX3 production could be significantly down-regulated by using the specific siRNA sequences for Jun N-terminal kinases (JNK). Furthermore, the activation of activator protein-1 (AP-1) was necessary for the up-regulation of PTX3 expression. We also found that the activation of nuclear factor-kappa B (NF-kappaB) played an important role in this process. Our findings demonstrate that SAA up-regulates PTX3 production via FPRL1 significantly, and thus, contributes to the inflammatory pathogenesis of atherosclerosis.
机译：血清淀粉样蛋白A（SAA）被认为是冠状动脉疾病中一种重要的急性期蛋白。然而，其参与动脉粥样硬化的免疫反应的了解很少。本研究旨在研究SAA对人主动脉内皮细胞（HAEC）中长五味素3（PTX3）的分泌的影响，后者是先天免疫的关键组成部分。我们的研究表明，重组SAA以显着的剂量和时间依赖性方式上调PTX3的产生，甲酰肽受体样1（FPRL1）的激活对于SAA诱导HAECs中PTX3的表达至关重要。同时，通过使用Jun N末端激酶（JNK）的特异性siRNA序列，可以显着下调SAA诱导的PTX3的产生。此外，激活蛋白1（AP-1）的激活对于PTX3表达的上调是必需的。我们还发现，核因子-κB（NF-kappaB）的激活在此过程中发挥了重要作用。我们的发现表明，SAA通过FPRL1显着上调PTX3的产生，从而促进了动脉粥样硬化的炎性发病机理。

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