| Literature DB >> 35551172 |
Shinya Yuge1, Koichi Nishiyama2,3, Yuichiro Arima4,5, Yasuyuki Hanada4,6, Eri Oguri-Nakamura1, Sanshiro Hanada4, Tomohiro Ishii1, Yuki Wakayama7, Urara Hasegawa8, Kazuya Tsujita9,10, Ryuji Yokokawa11, Takashi Miura12, Toshiki Itoh9,10, Kenichi Tsujita5, Naoki Mochizuki7, Shigetomo Fukuhara13.
Abstract
Angiogenesis is regulated in coordinated fashion by chemical and mechanical cues acting on endothelial cells (ECs). However, the mechanobiological mechanisms of angiogenesis remain unknown. Herein, we demonstrate a crucial role of blood flow-driven intraluminal pressure (IP) in regulating wound angiogenesis. During wound angiogenesis, blood flow-driven IP loading inhibits elongation of injured blood vessels located at sites upstream from blood flow, while downstream injured vessels actively elongate. In downstream injured vessels, F-BAR proteins, TOCA1 and CIP4, localize at leading edge of ECs to promote N-WASP-dependent Arp2/3 complex-mediated actin polymerization and front-rear polarization for vessel elongation. In contrast, IP loading expands upstream injured vessels and stretches ECs, preventing leading edge localization of TOCA1 and CIP4 to inhibit directed EC migration and vessel elongation. These data indicate that the TOCA family of F-BAR proteins are key actin regulatory proteins required for directed EC migration and sense mechanical cell stretching to regulate wound angiogenesis.Entities:
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Year: 2022 PMID： 35551172 PMCID： PMC9098626 DOI： 10.1038/s41467-022-30197-8
Source DB: PubMed Journal: Nat Commun ISSN： 2041-1723 Impact factor: 17.694