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TNF up-regulates Pentraxin3 expression in human airway smooth muscle cells via JNK and ERK1/2 MAPK pathways

机译:TNF通过JNK和ERK1 / 2 MAPK途径上调人气道平滑肌细胞中Pentraxin3的表达

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摘要

BackgroundLong pentraxin 3 (PTX3) is a novel candidate marker for inflammation in many chronic diseases. As a soluble pattern recognition receptor, PTX3 is involved in amplification of inflammatory reactions and regulation of innate immunity. Previously, we demonstrate that human airway smooth muscle cells (HASMC) express constitutively PTX3 and upon TNF stimulation. However, very little is known about the mechanism governing its expression in HASMC. We sought to investigate the mechanism governing TNF induced PTX3 expression in primary HASMC.
机译:背景长五味精3(PTX3)是许多慢性疾病中炎症的新型候选标记。作为可溶性模式识别受体,PTX3参与炎症反应的扩增和先天免疫的调节。以前,我们证明人气道平滑肌细胞(HASMC)组成型表达PTX3,并在TNF刺激下表达。但是,关于控制其在HASMC中表达的机制知之甚少。我们试图研究控制原发性HASMC中TNF诱导的PTX3表达的机制。

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