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Author  |
Sheikh, A.Q.; Taghian, T.; Hemingway, B.; Cho, H.; Kogan, A.B.; Narmoneva, D.A. |
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Title |
Regulation of endothelial MAPK/ERK signalling and capillary morphogenesis by low-amplitude electric field |
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Journal Article |
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2013 |
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Journal of the Royal Society, Interface / the Royal Society |
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10 |
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78 |
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20120548-20120548 |
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Keywords |
Animals; Apoptosis; Calcium; Calcium: metabolism; Capillaries; Capillaries: cytology; Capillaries: growth & development; Cell Proliferation; Cells; Cultured; Electromagnetic Fields; Extracellular Signal-Regulated MAP Kinases; Extracellular Signal-Regulated MAP Kinases: metabo; Gene Expression Regulation; MAP Kinase Kinase 4; MAP Kinase Kinase 4: metabolism; MAP Kinase Signaling System; Mice; Morphogenesis; Neovascularization; Phosphatidylinositol 3-Kinases; Phosphatidylinositol 3-Kinases: metabolism; Phosphorylation; Physiologic; Proto-Oncogene Proteins c-raf; Proto-Oncogene Proteins c-raf: metabolism; Time Factors; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor A: biosynthesis |
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Abstract |
Low-amplitude electric field (EF) is an important component of wound-healing response and can promote vascular tissue repair; however, the mechanisms of action on endothelium remain unclear. We hypothesized that physiological amplitude EF regulates angiogenic response of microvascular endothelial cells via activation of the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway. A custom set-up allowed non-thermal application of EF of high (7.5 GHz) and low (60 Hz) frequency. Cell responses following up to 24 h of EF exposure, including proliferation and apoptosis, capillary morphogenesis, vascular endothelial growth factor (VEGF) expression and MAPK pathways activation were quantified. A db/db mouse model of diabetic wound healing was used for in vivo validation. High-frequency EF enhanced capillary morphogenesis, VEGF release, MEK-cRaf complex formation, MEK and ERK phosphorylation, whereas no MAPK/JNK and MAPK/p38 pathways activation was observed. The endothelial response to EF did not require VEGF binding to VEGFR2 receptor. EF-induced MEK phosphorylation was reversed in the presence of MEK and Ca(2+) inhibitors, reduced by endothelial nitric oxide synthase inhibition, and did not depend on PI3K pathway activation. The results provide evidence for a novel intracellular mechanism for EF regulation of endothelial angiogenic response via frequency-sensitive MAPK/ERK pathway activation, with important implications for EF-based therapies for vascular tissue regeneration. |
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WP5 In vitro |
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UNIBAS @ david.schuermann @ |
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562 |
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