期刊
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
卷 40, 期 5, 页码 1495-1503出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/ijmm.2017.3143
关键词
Toll-like receptor 3/4; cytoskeleton; macrophage activation; vincristine; mitogen-activated protein kinase
资金
- National Natural Science Foundation of China [81472685, 81600469]
- Major Special Plan of Science and Technology of Shandong Province [2015ZDXX0802A01]
- Promotive Research Fund for Excellent Young and Middle-aged Scientisits of Shandong Province [BS2014YY037]
- Science and Technology Development Projects of Shandong Province [2016GSF201126]
Toll-like receptor 3 (TLR3) and TLR4 utilize adaptor proteins to activate mitogen-activated protein kinase (MAPK), resulting in the acute but transient inflammatory response aimed at the clearance of pathogens. In the present study, it was demonstrated that macrophage activation by lipopolysaccharide (LPS) or poly(I:C), leading to changes in cell morphology, differed significantly between the mouse macrophage cell line RAW264.7 and mouse primary peritoneal macrophages. Moreover, the expression of alpha- and beta-tubulin was markedly decreased following LPS stimulation. By contrast, alpha- and beta-tubulin expression were only mildly increased following poly(I:C) treatment. However, the expression of beta-actin and GAPDH was not significantly affected. Furthermore, it was verified that vincristine pretreatment abrogated the cytoskeleton rearrangement and decreased the synthesis and secretion of proinflammatory cytokines and migration of macrophages caused by LPS. Finally, it was observed that the MAPK/p38 signaling pathway regulating cytoskeleton rearrangement may participate in LPS-induced macrophage cytokine production and migration. Overall, the findings of the present study indicated that MAPK/p38 regulation of the cytoskeleton, particularly tubulin proteins, plays an important role in LPS-induced inflammatory responses via alleviating the synthesis and secretion of proinflammatory cytokines and inhibiting the migration of macrophages.
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