S1P promotes inflammation-induced tube formation by HLECs via the S1PR1/NF-κB pathway.
作者： Zhi Zheng , Yong-Zhi Zeng , Kun Ren , Xiao Zhu , Ying Tan
DOI: 10.1016/J.INTIMP.2018.11.032
关键词:
摘要: Abstract Inflammation-induced lymphangiogenesis is a widely accepted concept. However, most of the inflammatory factors and their related mechanisms have not been clarified. It has reported that sphingosine-1-phosphate (S1P) only closely to chronic process but also affects angiogenesis. Therefore, we investigated effects S1P on human lymphatic endothelial cells (HLECs). Our results showed promotes tumor necrosis factor-α (TNF-α) interleukin-1β (IL-1β) secretion in HLECs. We confirmed S1P-stimulated TNF-α IL-1β mediated through receptor 1 (S1PR1). Using siRNA siRNA, found play essential roles S1P-induced HLEC proliferation, migration, tube formation. induces phosphorylation NF-κB p65 activation nuclear translocation. A S1PR1 antagonist (W146) inhibitor (BAY11-7082) inhibited prevented Taken together, demonstrated for first time HLECs via S1PR1-mediated signaling pathways, thus affecting lymphangiogenesis. The study provides new strategy finding treatments lymphangiogenesis-related diseases.
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