Department of Neurosurgery, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Photochem Photobiol. 2011 Mar-Apr;87(2):441-6. doi: 10.1111/j.1751-1097.2010.00853.x. Epub 2010 Dec 10.
This study was designed to determine the in vitro angiogenic ability of far-infrared (FIR) radiation in the skin-derived cultured human microvascular endothelial cells and to elucidate the role of mitogen-activated protein kinases (MAPKs) in this process. The results revealed that FIR radiation from a WS(TM) TY301 FIR emitter activated p38 and extracellular signal-regulated kinase (ERK), but not Akt or c-Jun N-terminal protein kinases (JNK), and significantly promoted angiogenesis by increasing tube formation in Matrigel and the migration of cells across an eight micron polyester filter. The addition of 50 μM PD98059, a MEK inhibitor, significantly inhibited the activation of ERK and the enhanced angiogenesis; in contrast, the inhibition of p38 phosphorylation did not inhibit the enhanced angiogenesis. After FIR radiation, there was no increase in vascular endothelial growth factor (VEGF) isoforms (VEGF-A, -B, -C and -D) mRNA and VEGF protein, no increase phosphorylation of endothelial nitric oxide synthase (eNOS) detected using Western blotting, and no increase in NO production detected using flow cytometry in cells pre-incubated with the cell-permeable NO-binding dye diluted 4-amino-5-methylamino-2', 7'-difluorofluorescein diacetate (DAF-FM DA). This study revealed that FIR radiation possesses in vitro angiogenic activity via the activation of the MEK/ERK but not the VEGF/Akt/eNOS-dependent signaling pathways.
本研究旨在确定远红外（FIR）辐射在皮肤源性培养的人微血管内皮细胞中的体外血管生成能力，并阐明丝裂原激活蛋白激酶（MAPKs）在这一过程中的作用。结果表明，WS(TM)TY301 FIR 发射器产生的 FIR 辐射激活了 p38 和细胞外信号调节激酶（ERK），但不激活 Akt 或 c-Jun N 端蛋白激酶（JNK），并通过增加 Matrigel 中的管形成和细胞穿过 8 微米聚酯滤膜的迁移来显著促进血管生成。加入 50μM PD98059，一种 MEK 抑制剂，可显著抑制 ERK 的激活和增强的血管生成；相比之下，抑制 p38 磷酸化不会抑制增强的血管生成。FIR 辐射后，血管内皮生长因子（VEGF）异构体（VEGF-A、-B、-C 和 -D）mRNA 和 VEGF 蛋白没有增加，用 Western blot 检测到内皮型一氧化氮合酶（eNOS）的磷酸化没有增加，用流式细胞术检测到预先用可渗透细胞的 NO 结合染料稀释的 4-氨基-5-甲基氨基-2',7'-二氟荧光素二乙酸酯（DAF-FM DA）孵育的细胞中 NO 产量没有增加。本研究表明，FIR 辐射通过激活 MEK/ERK 而不是 VEGF/Akt/eNOS 依赖性信号通路具有体外血管生成活性。
