
혈관 내피 세포는 정수압 증가와 액틴 중합이라는 두 가지 기작을 동시에 활용하여 세포 이동과 새로운 혈관 형성을 촉진한다.


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Cell migration is a key process in the shaping and formation of tissues. During sprouting angiogenesis, endothelial tip cells invade avascular tissues by generating actomyosin-dependent forces that drive cell migration and vascular expansion. Surprisingly, ECs can still invade if actin polymerization is inhibited. In this study, we show that endothelial tip cells employ an alternative mechanism of cell migration that is dependent on Aquaporin (Aqp)-mediated water inflow and increase in hydrostatic pressure. In the zebrafish, ECs express aqp1a.1 and aqp8a.1 in newly formed vascular sprouts in a VEGFR2-dependent manner. Aqp1a.1 and Aqp8a.1 loss-of-function studies show an impairment in intersegmental vessels formation because of a decreased capacity of tip cells to increase their cytoplasmic volume and generate membrane protrusions, leading to delayed tip cell emergence from the dorsal aorta and slower migration. Further inhibition of actin polymerization resulted in a greater decrease in sprouting angiogenesis, indicating that ECs employ two mechanisms for robust cell migration in vivo . Our study highlights an important role of hydrostatic pressure in tissue morphogenesis.

### Competing Interest Statement

The authors have declared no competing interest.

Combined forces of hydrostatic pressure and actin polymerization drive endothelial tip cell migration and sprouting angiogenesis

혈관-내피-선단-세포-이동과-발아-혈관-신생에-있어-정수압과-액틴-중합이-미치는-결합된-힘


혈관 내피 선단 세포 이동과 발아 혈관 신생에 있어 정수압과 액틴 중합이 미치는 결합된 힘
