Tgf-beta regulation of suture morphogenesis and growth.
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.
Rawlins
Joseph T
JT
Department of Biomedical Sciences, Baylor College of Dentistry, Texas A&M Health Science Center, Dallas, Tex., USA.
Opperman
Lynne A
LA
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D002454:Cell Differentiation / Q000502:physiology; D049109:Cell Proliferation; D003393:Cranial Sutures / Q000254:growth & development* / Q000502:physiology; D003398:Craniosynostoses / Q000209:etiology / Q000503:physiopathology; D004195:Disease Models, Animal; D006801:Humans; D009024:Morphogenesis / Q000502:physiology*; D018125:Receptors, Transforming Growth Factor beta / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000145:classification / Q000502:physiology*
D018125:Receptors, Transforming Growth Factor beta; D016212:Transforming Growth Factor beta