scholarly journals Erk1/2 signaling is required for Tgf-β2–induced suture closure

2006 ◽  
Vol 235 (5) ◽  
pp. 1292-1299 ◽  
Author(s):  
Lynne A. Opperman ◽  
Claudia R. Fernandez ◽  
Sarah So ◽  
Joseph T. Rawlins
Keyword(s):  
2005 ◽  
Vol 116 (Supplement) ◽  
pp. 196-197
Author(s):  
Reha Yavuzer ◽  
Christopher Kelly ◽  
Noreen Durani ◽  
Vijay Mittal ◽  
Ian T. Jackson ◽  
...  

2016 ◽  
Vol 214 (1) ◽  
pp. S209
Author(s):  
Methodius Gamuo Tuuli ◽  
Molly J. Stout ◽  
Shannon Martin ◽  
Roxanne Rampersad ◽  
Alison G. Cahill ◽  
...  

2017 ◽  
Vol 44 ◽  
pp. 325-335 ◽  
Author(s):  
Maurizio Domanin ◽  
Adelaide Buora ◽  
Francesco Scardulla ◽  
Bruno Guerciotti ◽  
Laura Forzenigo ◽  
...  

1995 ◽  
Vol 83 (4) ◽  
pp. 575-582 ◽  
Author(s):  
Giuseppe Cinalli ◽  
Dominique Renier ◽  
Guy Sebag ◽  
Christian Sainte-Rose ◽  
Eric Arnaud ◽  
...  

✓ The incidence of chronic tonsillar herniation (CTH) was evaluated with magnetic resonance imaging in 44 patients with Crouzon's syndrome and 51 with Apert's syndrome; the incidence was 72.7% in Crouzon's syndrome and 1.9% in Apert's syndrome. All the patients with Crouzon's syndrome and progressive hydrocephalus had CTH, but of 32 individuals with Crouzon's syndrome and CTH, only 15 had progressive hydrocephalus. Five patients with Apert's syndrome were treated for progressive hydrocephalus; none had CTH. The patterns of suture closure in these two groups of patients were studied, and significant differences in coronal, sagittal, and lambdoid sutures were found between patients with Crouzon's and Apert's syndromes. In Crouzon's syndrome, significant differences in the pattern of lambdoid suture closure were found between the groups with and without CTH; in the group with CTH, the lambdoid closure appeared earlier. The authors propose that the high incidence of individuals with CTH who have Crouzon's syndrome is related to the premature synostosis of the lambdoid suture in the first 24 months of age.


2013 ◽  
Vol 61 (10) ◽  
pp. E1913
Author(s):  
Antonious Attallah ◽  
Prasanth Lingam ◽  
Joseph Chattahi ◽  
Janet Wyman ◽  
Adam Greenbaum ◽  
...  

Development ◽  
2000 ◽  
Vol 127 (9) ◽  
pp. 1845-1855 ◽  
Author(s):  
D.P. Rice ◽  
T. Aberg ◽  
Y. Chan ◽  
Z. Tang ◽  
P.J. Kettunen ◽  
...  

Mutations in the FGFR1-FGFR3 and TWIST genes are known to cause craniosynostosis, the former by constitutive activation and the latter by haploinsufficiency. Although clinically achieving the same end result, the premature fusion of the calvarial bones, it is not known whether these genes lie in the same or independent pathways during calvarial bone development and later in suture closure. We have previously shown that Fgfr2c is expressed at the osteogenic fronts of the developing calvarial bones and that, when FGF is applied via beads to the osteogenic fronts, suture closure is accelerated (Kim, H.-J., Rice, D. P. C., Kettunen, P. J. and Thesleff, I. (1998) Development 125, 1241–1251). In order to investigate further the role of FGF signalling during mouse calvarial bone and suture development, we have performed detailed expression analysis of the splicing variants of Fgfr1-Fgfr3 and Fgfr4, as well as their potential ligand Fgf2. The IIIc splice variants of Fgfr1-Fgfr3 as well as the IIIb variant of Fgfr2 being expressed by differentiating osteoblasts at the osteogenic fronts (E15). In comparison to Fgf9, Fgf2 showed a more restricted expression pattern being primarily expressed in the sutural mesenchyme between the osteogenic fronts. We also carried out a detailed expression analysis of the helix-loop-helix factors (HLH) Twist and Id1 during calvaria and suture development (E10-P6). Twist and Id1 were expressed by early preosteoblasts, in patterns that overlapped those of the FGF ligands, but as these cells differentiated their expression dramatically decreased. Signalling pathways were further studied in vitro, in E15 mouse calvarial explants. Beads soaked in FGF2 induced Twist and inhibited Bsp, a marker of functioning osteoblasts. Meanwhile, BMP2 upregulated Id1. Id1 is a dominant negative HLH thought to inhibit basic HLH such as Twist. In Drosophila, the FGF receptor FR1 is known to be downstream of Twist. We demonstrated that in Twist(+/)(−) mice, FGFR2 protein expression was altered. We propose a model of osteoblast differentiation integrating Twist and FGF in the same pathway, in which FGF acts both at early and late stages. Disruption of this pathway may lead to craniosynostosis.


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