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首页> 外文期刊>Cytokine >Wnt5a activates THP-1 monocytic cells via a β-catenin-independent pathway involving JNK and NF-κB activation
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Wnt5a activates THP-1 monocytic cells via a β-catenin-independent pathway involving JNK and NF-κB activation

机译：Wnt5a通过涉及JNK和NF-κB活化的β-catenin非依赖性途径活化THP-1单核细胞

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摘要

Wnt5a has been implicated in the activation of macrophages. However, the profile and mechanism of downstream regulation has not been characterized. In this study, we have investigated the regulation of Wnt5a-induced activation in monocytic THP-1 cells. Wnt5a activated THP-1 cells, enhancing adhesion to endothelial cells. Hypoxia induced the production of Wnt5a, suggesting a role in the hypoxia-induced activation of macrophages. Wnt5a induced the expression of various pro-inflammatory cytokines and inflammatory mediators, particularly IL8 and CXCL2, suggesting a major role in the secretion of CXC chemokines by macrophages. Wnt5a induced JNK phosphorylation and NF-κB activation via β-catenin-independent signaling. Interestingly, SP600125, a specific inhibitor of JNK, inhibited Wnt5a-induced activation of NF-κB, supporting JNK-dependent NF-κB activation. Our data suggest that Wnt5a activates monocytic cells via JNK and NF-κB activation.
机译：Wnt5a与巨噬细胞的激活有关。但是，下游调节的概况和机制尚未被表征。在这项研究中，我们研究了单核细胞THP-1细胞中Wnt5a诱导的激活的调控。 Wnt5a激活THP-1细胞，增强与内皮细胞的粘附。低氧诱导Wnt5a的产生，提示在低氧诱导的巨噬细胞激活中起作用。 Wnt5a诱导各种促炎细胞因子和炎性介质，特别是IL8和CXCL2的表达，表明巨噬细胞在CXC趋化因子的分泌中起主要作用。 Wnt5a通过不依赖β-连环蛋白的信号传导诱导JNK磷酸化和NF-κB活化。有趣的是，JNK的特异性抑制剂SP600125抑制Wnt5a诱导的NF-κB活化，支持JNK依赖性NF-κB活化。我们的数据表明Wnt5a通过JNK和NF-κB激活激活单核细胞。

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