Tgf-beta regulation of suture morphogenesis and growth.

J. Rawlins, L. Opperman
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引用次数: 17

Abstract

Premature suture obliteration results in an inability of cranial and facial bones to grow, with resulting craniofacial dysmorphology requiring surgical correction. Understanding the biological signaling associated with suture morphogenesis will enable less invasive treatment of patients with fused sutures, combined with therapy using biological molecules. While a number of advances have been made in identifying the genetic etiologies of various craniosynostotic syndromes, the pathogenesis of this condition is still not completely understood. Recently, it has been shown that differential expression of various transforming growth factor-beta (Tgf-beta) isoforms plays a crucial role in regulating suture patency once the sutures have formed. It has also been shown that differential expression of Tgf-beta isoforms may also play a role in craniosynostosis by altering proliferation, differentiation, and apoptosis within the suture. This chapter focuses on the role of Tgf-beta in suture morphogenesis and growth, exploring Tgf-beta biology, receptors, signaling pathways, animal models, and expression in both normal and pathological sutures.
tgf - β对缝线形态发生和生长的调控。
过早缝合闭塞导致颅面骨不能生长,导致颅面畸形需要手术矫正。了解与缝线形态发生相关的生物信号将使融合缝线患者的治疗更具侵入性,并结合使用生物分子治疗。虽然在确定各种颅缝闭合综合征的遗传病因方面取得了一些进展,但这种疾病的发病机制仍未完全了解。最近,研究表明,各种转化生长因子- β (tgf - β)异构体的差异表达在缝合线形成后调节缝合线通畅方面起着至关重要的作用。研究还表明,tgf - β亚型的差异表达也可能通过改变缝合线内的增殖、分化和凋亡而在颅缝闭合中发挥作用。本章重点关注tgf - β在缝线形态发生和生长中的作用,探讨tgf - β生物学、受体、信号通路、动物模型以及正常和病理缝线中的表达。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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