LL37 通过 ERK 信号通路诱导牙髓细胞中 VEGF 的表达。
LL37 induces VEGF expression in dental pulp cells through ERK signalling.
机构信息
Department of Periodontal Medicine, Applied Life Sciences, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Department of Oral Microbiology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.
出版信息
Int Endod J. 2015 Jul;48(7):673-9. doi: 10.1111/iej.12365. Epub 2014 Sep 12.
AIM
To examine the in vitro effects of LL37 on the expression of vascular endothelial growth factor (VEGF) in human pulp cells and to identify the intracellular signalling pathway involved.
METHODOLOGY
Pulp cells at passage 6 were treated with 10 μg mL(-1) synthesized LL37, and an inhibition assay was performed with MAPK or NF-κB inhibitors to determine the possible signalling pathway. VEGF mRNA, VEGF protein and phosphorylated ERK1/2 levels were determined by real-time PCR, ELISA and Western blot, respectively. Data were analysed using t-tests.
RESULTS
LL37 significantly increased both the mRNA and protein levels of VEGF in pulp cells (P < 0.01). However, pre-treatment with an ERK kinase inhibitor suppressed these increases. Furthermore, the inhibitor blocked LL37-induced ERK1/2 phosphorylation.
CONCLUSIONS
LL37 activated the ERK pathway to boost VEGF secretion from human pulp cells. Because of this angiogenic effect and its reported induction of pulp cell migration and antimicrobial activity against cariogenic bacteria, LL37 may be applicable as a pulp capping material.
目的
研究 LL37 对人牙髓细胞血管内皮生长因子（VEGF）表达的体外影响，并确定涉及的细胞内信号通路。
方法
用 10μg/mL 合成的 LL37 处理第 6 代牙髓细胞，并使用 MAPK 或 NF-κB 抑制剂进行抑制试验，以确定可能的信号通路。通过实时 PCR、ELISA 和 Western blot 分别测定 VEGF mRNA、VEGF 蛋白和磷酸化 ERK1/2 水平。使用 t 检验分析数据。
结果
LL37 显著增加了牙髓细胞中 VEGF 的 mRNA 和蛋白水平（P<0.01）。然而，ERK 激酶抑制剂的预处理抑制了这些增加。此外，该抑制剂阻断了 LL37 诱导的 ERK1/2 磷酸化。
结论
LL37 通过激活 ERK 通路来促进人牙髓细胞中 VEGF 的分泌。由于这种血管生成作用及其对牙髓细胞迁移的诱导作用和对致龋细菌的抗菌活性，LL37 可用作牙髓盖髓材料。
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