Notch signaling in skeletal stem cells.
Notch signaling in skeletal stem cells.
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DOI：
10.1007/s00223-013-9773-z
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发表时间：
2014-01
影响因子：
4.2
通讯作者：
Bae, Yangjin
中科院分区：
文献类型：
--
作者：
Chen, Shan;Lee, Brendan H.;Bae, Yangjin
骨骼起源于干细胞居住在硬结和神经嵴，经历增殖，迁移和承诺。骨骼干细胞的发育受到许多信号通路的影响，这些信号通路支配细胞命运决定、增殖、分化和凋亡。本文就Notch信号在调节骨骼系统不同细胞类型中的作用以及它们之间的相互作用进行综述。骨软骨祖细胞需要Notch信号来维持多能性并防止过早分化为成骨细胞。随后，Notch信号的过度激活抑制成骨细胞成熟。此外，骨软骨祖细胞中的Notch信号传导是软骨细胞增殖、肥大和抑制终末分化所必需的。翻译研究表明，Notch信号在骨肉瘤和骨关节炎中起着至关重要的作用，这些疾病中经常重复来自发育途径的概念。这带来了利用从发育中学到的分子机制来接近异常骨/软骨代谢或肿瘤发生的病理过程的希望。以组织特异性方式靶向Notch受体或配体的药理学试剂将为治疗由Notch信号传导失调引起的骨/软骨疾病提供新的机会。
The skeleton is originated from stem cells residing in the sclerotome and neural crest that undergo proliferation, migration and commitment. The development of the skeletal stem cells is influenced by many signaling pathways that govern cell fate determination, proliferation, differentiation and apoptosis. This review will focus on Notch signaling functions in regulating different cells types forming the skeletal system as well as the interplay between them to maintain homeostasis. Osteochondroprogenitors require Notch signaling to maintain the multipotency and to prevent from premature differentiation into osteoblast. Subsequently, over-activation of Notch signaling suppresses osteoblast maturation. Moreover, Notch signaling in osteochondroprogenitors is required for chondrocyte proliferation, hypertrophy and suppresses terminal differentiation. Translational studies demonstrated a crucial role of Notch signaling in osteosarcoma and osteoarthritis, where concepts derived from developmental pathways are often recapitulated. This brings hope of taking advantages of the molecular mechanisms learned from development to approach the pathological processes underlying abnormal bone/cartilage metabolism or tumorigenesis. Pharmacological agents that target Notch receptors or ligands in a tissue specific fashion would offer new opportunities for treating bone/cartilage diseases caused by dysregulation of Notch signaling.
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