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适度的流体切应力可以通过激活 FAK-MEK5-ERK5-cFos-AP1 信号通路来调节核髓核和周围炎症介质的细胞骨架。

Moderate Fluid Shear Stress Could Regulate the Cytoskeleton of Nucleus Pulposus and Surrounding Inflammatory Mediators by Activating the FAK-MEK5-ERK5-cFos-AP1 Signaling Pathway.

机构信息

Guangzhou City Red Cross Hospital, The Fourth Affiliated Hospital of Medical College, Jinan University, Guangzhou 510220, China.

出版信息

Dis Markers. 2018 Jun 12;2018:9405738. doi: 10.1155/2018/9405738. eCollection 2018.

DOI:10.1155/2018/9405738
PMID:30008976
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6020454/
Abstract

We first applied moderate fluid shear stress to nucleus pulposus cells. The correlation of AP-1 with type II collagen, proteoglycan, Cytokeratin 8 protein, MAP-1, MAP-2, and MAP-4 and the correlation of AP-1 with IL-1, TNF-, IL-6, IL-8, MIP-1, MCP-1, and NO were detected. Our results document that moderate fluid shear stress could activate the FAK-MEK5-ERK5-cFos-AP1 signaling pathway. AP1 could downregulate the construct factors of cytoskeleton such as type II collagen, proteoglycan, Cytokeratin 8 protein, MAP-1, MAP-2, and MAP-4 in nucleus pulposus cell after the fluid shear stress was loaded. AP1 could upregulate the inflammatory factors such as IL-1, TNF-, IL-6, IL-8, MIP-1, MCP-1, and NO in nucleus pulposus cell after the fluid shear stress was loaded. Taken together, our data suggested that moderate fluid shear stress may play an important role in the cytoskeleton of nucleus pulposus and surrounding inflammatory mediators by activating the FAK-MEK5-ERK5-cFos-AP1 signaling pathway, thereby affecting cell degeneration.

摘要

我们首先对髓核细胞施加适度的流体剪切应力。检测了 AP-1 与 II 型胶原、蛋白聚糖、细胞角蛋白 8 蛋白、MAP-1、MAP-2 和 MAP-4 的相关性，以及 AP-1 与 IL-1、TNF-、IL-6、IL-8、MIP-1、MCP-1 和 NO 的相关性。我们的结果表明，适度的流体剪切应力可以激活 FAK-MEK5-ERK5-cFos-AP1 信号通路。在加载流体剪切应力后，AP1 可以下调髓核细胞中的细胞骨架构建因子，如 II 型胶原、蛋白聚糖、细胞角蛋白 8 蛋白、MAP-1、MAP-2 和 MAP-4。AP1 可以上调 IL-1、TNF-、IL-6、IL-8、MIP-1、MCP-1 和 NO 等炎症因子在髓核细胞中的表达。总之，我们的数据表明，适度的流体剪切应力可能通过激活 FAK-MEK5-ERK5-cFos-AP1 信号通路，在髓核及其周围的炎症介质的细胞骨架中发挥重要作用，从而影响细胞的退变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1a5/6020454/342bb931032a/DM2018-9405738.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1a5/6020454/550fbdb3ef1f/DM2018-9405738.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1a5/6020454/eb2f38cef8f5/DM2018-9405738.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1a5/6020454/a2c51fe0b416/DM2018-9405738.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1a5/6020454/342bb931032a/DM2018-9405738.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1a5/6020454/550fbdb3ef1f/DM2018-9405738.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1a5/6020454/eb2f38cef8f5/DM2018-9405738.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1a5/6020454/a2c51fe0b416/DM2018-9405738.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1a5/6020454/342bb931032a/DM2018-9405738.004.jpg

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