MAPK Signaling Is Required for LPs-induced VEGF in Pulp Stem Cells
MAPK Signaling Is Required for LPs-induced VEGF in Pulp Stem Cells
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DOI：
10.1177/0022034509357556
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发表时间：
2010-03-01
影响因子：
7.6
通讯作者：
Noer, J. E.
中科院分区：
文献类型：
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作者：
Botero, T. M.;Son, J. S.;Noer, J. E.
龋齿引起的牙髓炎通常伴随着牙髓微血管密度的增加。然而，牙髓细胞识别脂多糖（LPS）的机制仍不清楚。我们假设牙髓卟啉单胞菌和大肠杆菌LPS通过丝裂原活化蛋白激酶（MAPK）信号转导诱导牙髓干细胞（DPSC）和人牙髓成纤维细胞（HDPF）中血管内皮生长因子（VEGF）的表达。采用ELISA、半定量RT-PCR、免疫荧光和Western印迹法。在此，我们观察到LPS诱导DPSC和HDPF细胞中的VEGF表达，并且两种细胞类型均表达Toll样受体4（TLR-4）。值得注意的是，LPS诱导的VEGF与蛋白激酶C（PKC zeta）和细胞外信号调节激酶（ERK 1/2）的磷酸化相关，并且依赖于MAPK活化。这些数据的分析，共同揭示了一个信号通路负责合成的血管内皮生长因子的牙髓细胞，并提出了一种新的治疗目标，在牙齿牙髓炎的血管反应的管理。
Caries-induced pulpitis is typically accompanied by an increase in dental pulp microvascular density. However, the mechanisms by which dental pulp cells recognize lipopolysaccharides (LPSs) remain unclear. We hypothesized that Porphyromonas endodontalis and Escherichia coli LPSs induce vascular endothelial growth factor (VEGF) expression in dental pulp stem cells (DPSC) and human dental pulp fibroblasts (HDPF) through mitogen-activated protein kinase (MAPK) signaling. ELISA, semi-quantitative RT-PCR, immunofluorescence, and Western blots were used. Here, we observed that LPSs induced VEGF expression in DPSC and HDPF cells, and both cell types express Toll-like receptor 4 (TLR-4). Notably, LPS-induced VEGF is associated with phosphorylation of protein kinase C (PKC zeta) and extracellular signal-regulator kinase (ERK1/2) and is dependent upon MAPK activation. Analysis of these data, collectively, unveils a signaling pathway responsible for synthesis of VEGF by pulp cells and suggests a novel therapeutic target for the management of vascular responses in teeth with pulpitis.