Electrical stimulation facilitates the angiogenesis of human umbilical vein endothelial cells through MAPK/ERK signaling pathway by stimulating FGF2 secretion
Electrical stimulation facilitates the angiogenesis of human umbilical vein endothelial cells through MAPK/ERK signaling pathway by stimulating FGF2 secretion
复制标题
电刺激促进人脐静脉内皮细胞分泌FGF 2通过MAPK/ERK信号通路促进血管生成
DOI：
10.1152/ajpcell.00474.2018
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发表时间：
2019-08-01
影响因子：
5.5
通讯作者：
Yan, Hong
中科院分区：
文献类型：
--
作者：
Geng, Kang;Wang, Jing;Yan, Hong
电刺激（ES）能够通过刺激成纤维细胞来促进血管生成。成纤维细胞生长因子2 （FGF2）是一种独立的血管生成诱导剂。本研究旨在通过丝裂原活化蛋白激酶/细胞外信号调节激酶（MAPK/ERK）信号通路，评估es诱导的FGF2分泌在伤口愈合过程中影响血管生成的作用。将成纤维细胞和人脐静脉内皮细胞（HUVECs）暴露于ES，并将HUVECs与ES处理的成纤维细胞培养液共培养。ES暴露对成纤维细胞或huvec没有毒性作用。ES可促进成纤维细胞和huvec的生长以及FGF2的分泌。这是通过NOS途径诱导的。es诱导的FGF2分泌可增加血管内皮生长因子（VEGF）蛋白并促进迁移。侵袭和血管生成。此外，es诱导的FGF2分泌激活了MAPK/ERK信号通路。然而，抑制MAPK/ERK信号通路逆转了es诱导的FGF2分泌的积极作用。体外实验表明，ES对伤口愈合有积极作用。综上所述，研究结果表明，ES促进FGF2分泌，进而激活MAPK/ERK信号通路，促进血管生成，促进伤口愈合。
Electrical stimulation (ES) is able to enhance angiogenesis by stimulating fibroblasts. Fibroblast growth factor 2 (FGF2) is an independent angiogenesis inducer. The present study aimed to evaluate the role of ES-induced FGF2 secretion in affecting angiogenesis during wound healing via the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling pathway. Fibroblasts and human umbilical vein endothelial cells (HUVECs) were exposed to ES, and the HUVECs were cocultured with ES-treated fibroblast culture solution. ES exposure showed no toxic effects on fibroblasts or HUVECs. ES led to enhanced growth of fibroblasts and HUVECs as well as FGF2 secretion. which is induced through the NOS pathway. ES-induced FGF2 secretion was shown to increase vascular endothelial growth factor (VEGF) protein and enhance migration. invasion, and angiogenesis of HUVECs. Also, ES-induced FGF2 secretion activated the MAPK/ERK signaling pathway. However, inhibition of the MAPK/ERK signaling pathway reversed the positive effects of ES-induced FGF2 secretion. In vitro experiments showed positive effects of ES on wound healing. Taken together, the findings suggested that ES promoted FGF2 secretion and then activated the MAPK/ERK signaling pathway by facilitating angiogenesis and promoting wound healing.