Cell reports · 2021
Mechanical load regulates bone growth via periosteal Osteocrin.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Watanabe-Takano Haruko, Ochi Hiroki, Chiba Ayano, Matsuo Ayaka, Kanai Yugo, Fukuhara Shigetomo, Ito Naoki, Sako Keisuke, Miyazaki Takahiro, Tainaka Kazuki, Harada Ichiro, Sato Shingo, Sawada Yasuhiro, Minamino Naoto, Takeda Shu, Ueda Hiroki R, Yasoda Akihiro, Mochizuki Naoki
Аннотация
Mechanical stimuli including loading after birth promote bone growth. However, little is known about how mechanical force triggers biochemical signals to regulate bone growth. Here, we identified a periosteal-osteoblast-derived secretory peptide, Osteocrin (OSTN), as a mechanotransducer involved in load-induced long bone growth. OSTN produced by periosteal osteoblasts regulates growth plate growth by enhancing C-type natriuretic peptide (CNP)-dependent proliferation and maturation of chondrocytes, leading to elongation of long bones. Additionally, OSTN cooperates with CNP to regulate bone formation. CNP stimulates osteogenic differentiation of periosteal osteoprogenitors to induce bone formation. OSTN binds to natriuretic peptide receptor 3 (NPR3) in periosteal osteoprogenitors, thereby preventing NPR3-mediated clearance of CNP and consequently facilitating CNP-signal-mediated bone growth. Importantly, physiological loading induces Ostn expression in periosteal osteoblasts by suppressing Forkhead box protein O1 (FoxO1) transcription factor. Thus, this study reveals a crucial role of OSTN as a mechanotransducer converting mechanical loading to CNP-dependent bone formation.