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Wnt5a promotes inflammatory responses via nuclear factor κB (NF-κB) and mitogen-activated protein kinase (MAPK) pathways in human dental pulp cells.

作者信息

Zhao Yuan, Wang Chen-Lin, Li Rui-Min, Hui Tian-Qian, Su Ying-Ying, Yuan Quan, Zhou Xue-Dong, Ye Ling

出版信息

J Biol Chem. 2017 Mar 10;292(10):4358. doi: 10.1074/jbc.A113.546523.

DOI:10.1074/jbc.A113.546523
PMID:28283587
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5354512/
Abstract
摘要

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1
Wnt5a promotes inflammatory responses via nuclear factor κB (NF-κB) and mitogen-activated protein kinase (MAPK) pathways in human dental pulp cells.Wnt5a通过核因子κB（NF-κB）和丝裂原活化蛋白激酶（MAPK）途径促进人牙髓细胞中的炎症反应。
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2
Lipopolysaccharide enhances Wnt5a expression through toll-like receptor 4, myeloid differentiating factor 88, phosphatidylinositol 3-OH kinase/AKT and nuclear factor kappa B pathways in human dental pulp stem cells.脂多糖通过Toll样受体4、髓样分化因子88、磷脂酰肌醇3-羟基激酶/蛋白激酶B和核因子κB信号通路增强人牙髓干细胞中Wnt5a的表达。
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Anti-inflammatory effects of glutamine on LPS-stimulated human dental pulp cells correlate with activation of MKP-1 and attenuation of the MAPK and NF-κB pathways.谷氨酰胺对脂多糖刺激的人牙髓细胞的抗炎作用与丝裂原活化蛋白激酶磷酸酶-1的激活以及丝裂原活化蛋白激酶和核因子κB信号通路的减弱相关。
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siRNA-mediated silencing of Wnt5a regulates inflammatory responses in atherosclerosis through the MAPK/NF-κB pathways.小干扰RNA介导的Wnt5a沉默通过丝裂原活化蛋白激酶/核因子κB信号通路调节动脉粥样硬化中的炎症反应。
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