Hydrostatic pressure promotes endothelial tube formation through aquaporin 1 and Ras-ERK signaling

Daisuke Yoshino, Kenichi Funamoto, Kakeru Sato, Kenry, Masaaki Sato, Chwee Teck Lim

Research output: Contribution to journalArticlepeer-review

23 Citations (Scopus)


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.

Original languageEnglish
Article number152
JournalCommunications Biology
Issue number1
Publication statusPublished - 2020 Dec 1


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