Hydrostatic pressure promotes endothelial tubulogenesis

Written by Ebony Torrington

Researchers from Tokyo University of Agriculture and Technology (Tokyo, Japan) have discovered a mechanism by which the endothelial cells lining the inside of blood vessels are stimulated. The findings, published in Communications Biology, may lead to new treatments to help regenerate blood vessels in degenerative diseases.

The team studied how endothelial cells lining the inside of blood vessels regenerated in response to hydrostatic pressure.

“Blood vessels are constantly exposed to stimuli such as fluid shear stress, cyclic tensile force and hydrostatic pressure,” explained. Daisuke Yoshino (Tokyo University of Agriculture and Technology).

“Although the detailed mechanisms about cellular responses to shear stress and tensile force have been studied, we have not well understood how hydrostatic pressure affects vascular function.”

To understand how endothelial cells sense hydrostatic pressure and convert it into biological signals, which induce endothelial tubular responses, the research team applied pressure to the endothelial cells. It was found that the increase in pressure activated water transfer through the channel aquaporin 1. Aquaporin 1 stimulated the protein signaling channel Ras-ERK.

The process stimulated endothelial cell growth; the research team believe this to be a clear connection between pressure stimulation and intracellular biochemical signals.

“Our ultimate goal is to comprehensively clarify how the mechanisms described in this study are altered by differences in the blood pressure conditions, such as local conditions, magnitude and mode by which it is exerted,” concluded Yoshino. “We hope the clarified mechanisms will lead to the development of new treatments for diseases invoking abnormalities in vascular formation, such as venous malformations.”

Source: Yoshino D, Funamoto K, Sato K, Kenry, Sato M, Teck Lim C. Hydrostatic pressure promotes endothelial tube formation through aquaporin 1 and Ras-ERK signaling. Commun. Biol. 3, 152 (2020).