Electric current-induced lymphatic activation

The lymphatic system in skin plays important roles in drainage of wastes and in the afferent phase of immune response. We previously showed that activation of vascular endothelial growth factor receptor (VEGFR), specifically the VEGFC/VEGFR‐3 pathway, attenuates oedema and inflammation by promoting...

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Bibliographic Details
Published in:Experimental dermatology 2014-12, Vol.23 (12), p.936-938
Main Authors: Kajiya, Kentaro, Matsumoto-Okazaki, Yuko, Sawane, Mika, Fukada, Kaedeko, Takasugi, Yuya, Akai, Tomonori, Saito, Naoki, Mori, Yuichiro
Format: Article
Language:English
Subjects:
calcium influx
Calcium Signaling
Cell Movement
Cell Proliferation
Cells, Cultured
Cytoskeleton - physiology
direct current
Electric Stimulation
Endothelial Cells - cytology
Endothelial Cells - physiology
Focal Adhesion Kinase 1 - physiology
Humans
lymphatic
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Summary:The lymphatic system in skin plays important roles in drainage of wastes and in the afferent phase of immune response. We previously showed that activation of vascular endothelial growth factor receptor (VEGFR), specifically the VEGFC/VEGFR‐3 pathway, attenuates oedema and inflammation by promoting lymphangiogenesis, suggesting a protective role of lymphatic vessels against skin inflammation. However, it remains unknown how physical stimuli promote lymphatic function. Here, we show that lymphatic endothelial cells (LECs) are activated by direct‐current (DC) electrical stimulation, which induced extension of actin filaments of LECs, increased calcium influx into LECs, and increased phosphorylation of p38 mitogen‐activated protein kinase (MAPK). An inhibitor of focal adhesion kinase, which plays a role in cellular adhesion and motility, diminished the DC‐induced extension of F‐actin and abrogated p38 phosphorylation. Time‐lapse imaging revealed that pulsed‐DC stimulation promoted proliferation and migration of LECs. Overall, these results indicate that electro‐stimulation activates lymphatic function by activating p38 MAPK.
ISSN:0906-6705
1600-0625
DOI:10.1111/exd.12562