Angiogenic Signaling Triggered by Cariogenic Bacteria in Pulp Cells
Angiogenic Signaling Triggered by Cariogenic Bacteria in Pulp Cells
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DOI：
10.1177/0022034509341946
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发表时间：
2009-09-01
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：
Soden, R. I.;Botero, T. M.;Noer, J. E.
在深龋病患牙的牙髓中观察到的炎症以血管密度显著增加为特征。已知革兰氏阳性致龋菌的脂磷壁酸(LTA)可诱导牙髓细胞表达血管内皮生长因子(VEGF)。本研究的假设是LTA通过TLR2和PI3K/Akt信号通路诱导牙髓细胞表达血管内皮生长因子。用血链球菌LTA刺激成牙本质细胞样细胞(MDPC-23)和未分化牙髓细胞(OD-21)，观察TLR2、PI3K/Akt和IKK信号通路在LTA诱导的血管内皮生长因子(VEGF)表达中的作用。这些研究表明，TLR2信号途径通过PI3K-Akt通路是LTA诱导牙髓细胞表达血管内皮生长因子所必需的。相反，抑制IKK信号并不能阻止LTA对血管内皮细胞生长因子的上调。了解致龋菌触发的信号通路可能为牙髓炎的临床治疗提供新的治疗靶点。
The inflammation observed in the dental pulp of teeth with deep caries lesions is characterized by a significant increase in blood vessel density. It is known that lipoteichoic acid (LTA) from Gram-positive cariogenic bacteria induces expression of vascular endothelial growth factor (VEGF) in dental pulp cells. The hypothesis underlying this study was that LTA induces VEGF expression in dental pulp cells through TLR2 and PI3k/Akt signaling. Odontoblast-like cells (MDPC-23) and undifferentiated pulp cells (OD-21) were exposed to LTA from Streptococcus sanguis, and the role of TLR2, PI3K/Akt, and IKK signaling in LTA-induced VEGF expression was evaluated. These studies demonstrated that TLR2 signaling through the PI3K-Akt pathway is necessary for LTA-induced VEGF expression in pulp cells. In contrast, inhibition of IKK signaling did not prevent VEGF up-regulation in response to LTA. Understanding signaling pathways triggered by cariogenic bacteria may reveal novel therapeutic targets for the clinical management of pulpitis.