Yoshino Daisuke, Sato Masaaki
Frontier Research Institute forInterdisciplinary Sciences,Tohoku University,6-3 Aramaki-Aoba, Aoba,Sendai 980-8578, Japane-mail:
Frontier Research Institute forInterdisciplinary Sciences,Tohoku University,6-3 Aramaki-Aoba, Aoba,Sendai 980-8578, Japan.
J Biomech Eng. 2019 Sep 1;141(9). doi: 10.1115/1.4044046.
Blood pressure is an important factor both in maintaining body homeostasis and in its disruption. Vascular endothelial cells (ECs) are exposed to varying degrees of blood pressure and therefore play an important role in these physiological and pathological events. However, the effect of blood pressure on EC functions remains to be elucidated. In particular, we do not know how ECs sense and respond to changes in hydrostatic pressure even though the hydrostatic pressure is known to affect the EC functions. Here, we hypothesized that the cellular responses, leading to the reported pressure effects, occur at an early stage of pressure exposure and observed the early-stage dynamics in ECs to elucidate mechanisms through which ECs sense and respond to hydrostatic pressure. We found that exposure to hydrostatic pressure causes an early actomyosin-mediated contraction of ECs without a change in cell morphology. This response could be caused by water efflux from the ECs following exposure to hydrostatic pressure. Although only a limited study, these findings do explain a part of the mechanism through which ECs sense and respond to hydrostatic pressure.
血压在维持身体内稳态及其破坏过程中都是一个重要因素。血管内皮细胞（ECs）会受到不同程度的血压影响，因此在这些生理和病理过程中发挥着重要作用。然而，血压对内皮细胞功能的影响仍有待阐明。特别是，尽管已知流体静压会影响内皮细胞功能，但我们并不清楚内皮细胞如何感知并响应流体静压的变化。在此，我们假设导致所报道的压力效应的细胞反应发生在压力暴露的早期阶段，并观察了内皮细胞的早期动态变化，以阐明内皮细胞感知和响应流体静压的机制。我们发现，暴露于流体静压会导致内皮细胞早期发生肌动球蛋白介导的收缩，而细胞形态没有变化。这种反应可能是由于暴露于流体静压后内皮细胞中的水分外流所致。尽管只是一项有限的研究，但这些发现确实解释了内皮细胞感知和响应流体静压的部分机制。
