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Title: Hydrostatic pressure promotes endothelial tube formation through aquaporin 1 and Ras-ERK signaling
Authors: Yoshino, D.
Funamoto, K.
Sato, K.
Sato, M.
Lim, C.T. 
Issue Date: 2020
Publisher: Nature Research
Citation: Yoshino, D., Funamoto, K., Sato, K., Kenry, Sato, M., Lim, C.T. (2020). Hydrostatic pressure promotes endothelial tube formation through aquaporin 1 and Ras-ERK signaling. Communications Biology 3 (1) : 152. ScholarBank@NUS Repository.
Rights: Attribution 4.0 International
Abstract: Vascular tubulogenesis is tightly linked with physiological and pathological events in the living body. Endothelial cells (ECs), which are constantly exposed to hemodynamic forces, play a key role in tubulogenesis. Hydrostatic pressure in particular has been shown to elicit biophysical and biochemical responses leading to EC-mediated tubulogenesis. However, the relationship between tubulogenesis and hydrostatic pressure remains to be elucidated. Here, we propose a specific mechanism through which hydrostatic pressure promotes tubulogenesis. We show that pressure exposure transiently activates the Ras/extracellular signal-regulated kinase (ERK) pathway in ECs, inducing endothelial tubulogenic responses. Water efflux through aquaporin 1 and activation of protein kinase C via specific G protein–coupled receptors are essential to the pressure-induced transient activation of the Ras/ERK pathway. Our approach could provide a basis for elucidating the mechanopathology of tubulogenesis-related diseases and the development of mechanotherapies for improving human health. © 2020, The Author(s).
Source Title: Communications Biology
ISSN: 2399-3642
DOI: 10.1038/s42003-020-0881-9
Rights: Attribution 4.0 International
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