Electromagnetic Wave Irradiation Promotes Osteoblastic Cell Proliferation and Up-Regulates Growth Factors via Activation of the ERK1/2 and p38 MAPK Pathways
Electromagnetic Wave Irradiation Promotes Osteoblastic Cell Proliferation and Up-Regulates Growth Factors via Activation of the ERK1/2 and p38 MAPK Pathways
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DOI：
10.1159/000369722
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发表时间：
2015-01-01
影响因子：
--
通讯作者：
Matsuo, Takashi
中科院分区：
文献类型：
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作者：
Yumoto, Hiromichi;Hirao, Kouji;Matsuo, Takashi
背景/目的：牙周炎伴骨吸收是由细菌感染引起的炎症反应。我们最近报道了电磁波辐射（EMWI）具有杀菌作用。然而，EMWI对牙周组织的影响尚不清楚。本研究旨在探讨EMWI对成骨细胞的影响。方法：采用EMWI（500 ~ 1，000 kHz，5次，1 sec/次）对成骨细胞MC 3 T3-E1进行处理。细胞生长和细胞毒性分别通过细胞增殖试验和乳酸脱氢酶释放的测量来确定。分别用实时荧光PCR和艾尔莎分析生长因子的基因表达和蛋白质产生。通过免疫印迹和特异性抑制剂阻断试验研究EMWI激活的细胞信号转导途径。结果：EMWI后3d成骨细胞增殖明显增强，未观察到细胞毒性。EMWI上调多种生长因子，如血管内皮生长因子（VEGF）和血小板衍生生长因子（PDGF）。EMWI可在5 min内诱导ERK 1/2、p38 MARK和SAPK/JNK磷酸化，MARK特异性抑制剂可部分抑制PDGF-AA和VEGF的生成。结论：这些结果表明EMWI通过ERK 1/2和p38 MAPK途径增加成骨细胞活性和生长因子的表达，并表明EMWI可能有利于骨组织修复，如牙周炎。版权所有（C）2015 S. Karger AG，巴塞尔
Background/Aims: Periodontitis with bone resorption is caused by inflammatory reactions to bacterial infection. We recently reported that electromagnetic wave irradiation (EMWI) has bactericidal effects. However, the effects of EMWI on periodontal tissues remain unclear. This study was aimed to investigate the effects of EMWI on osteoblasts. Methods: Osteoblastic cells MC3T3-E1 were treated with EMWI (500-1,000 kHz, 5 times, 1 sec/time). Cell growth and cytotoxicity were determined by cell proliferation assays and measurement of lactate dehydrogenase release, respectively. Gene expression and protein production of growth factors were analyzed using real-time PCR and ELSA, respectively. EMWI-activated cellular signal transduction pathways were investigated by immunoblotting and blocking assay with specific inhibitors. Results: Osteoblasts proliferation was significantly enhanced 3 days after EMWI and no cytotoxicity was observed. EMWI up-regulated various growth factors, such as vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF). EMWI induced ERK1/2, p38 MARK and SAPK/JNK phosphorylation within 5 min, and the production of PDGF-AA and VEGF was partially reduced by MARK-specific inhibitor. Conclusion: These findings demonstrated that EMWI increases osteoblastic cell activity and the expression of growth factors via ERK1/2 and p38 MAPK pathways and suggested that EMWI may be beneficial to bone tissue repair such as periodontitis. Copyright (C) 2015 S. Karger AG, Basel