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Epithelial Fibroblast Growth Factor Receptor 1 Regulates Enamel Formation
K. Takamori1,2,
R. Hosokawa1,
X. Xu1,
X. Deng1,
P. Bringas, Jr.1 and
Y. Chai1,*
1 Center for Craniofacial Molecular Biology, School of Dentistry, University of Southern California, 2250 Alcazar Street, CSA 103, Los Angeles, CA 90033, USA; and
2 Division of Pediatric Dentistry, Department of Human Development & Fostering, Meikai University School of Dentistry, 1-1 Keyaki-dai, Sakado, Saitama, 350-0283, Japan

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Figure 1. Microscopic phenotype of K14-Cre;Fgfr1fl/fl newborn mice. LacZ staining of K14-Cre;R26R newborn mice (A). Black arrow indicates ameloblasts, black arrowhead indicates cervical loop, and * indicates tip of incisor. Hematoxylin-eosin sections of control (K14-Cre;Fgfr1fl/+) (B,D-G) and K14-Cre;Fgfr1fl/fl (C,H-K) newborn mice. D-K are enlarged from the boxes in B and C, showing the cervical loop (D,H), proliferating stage (E,I), enamel-secretory stage (F,J), and maturation stage (G,K). (K) White arrowheads indicate the dentin-enamel junction. Black arrowheads indicate the surface of the broken enamel structure. Black arrows indicate the lava-like structure. A, ameloblast; D, dentin; E, enamel; O, odontoblast; *, the tip of incisor.
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Figure 2. Phenotypic analysis of K14-Cre;Fgfr1fl/fl mice. In situ hybridization of Fgfr1 (A,B) and Amelogenin mRNA (C,D) and immunostaining of Amelogenin (E,F) and E-cadherin (G,H) in K14-Cre;Fgfr1fl/+ (control) (A,C,E,G) and K14-Cre;Fgfr1fl/fl (B,D,F,H) mice. (A) In control mice, Fgfr1 is expressed in ameloblasts (black arrowheads) and odontoblasts (black arrows). (B) In K14-Cre;Fgfr1fl/fl mice, Fgfr1 is not detectable in ameloblasts (*), although it is expressed in odontoblasts and surrounding bone (black arrows). (C,D) Amelogenin expression is indistinguishable in control and K14-Cre;Fgfr1fl/fl mice. (E,F) Amelogenin expression is strongly localized in the control mice (E, black arrowheads), but not in K14-Cre;Fgfr1fl/fl mice (F, white arrowheads). (G,H) Enamel-secreting ameloblasts contain an E-cadherin-negative area (*) in control mice, but the pattern is altered in K14-Cre;Fgfr1fl/fl mice. A, ameloblast; D, dentin; E, enamel; O, odontoblast.
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Figure 3. Phenotypic analysis of K14-Cre;Fgfr1fl/fl adult mice. Mandibular incisor surfaces of K14-Cre;Fgfr1fl/+ (control) and K14-Cre;Fgfr1fl/fl mice at 8 wks after birth observed by objective microscopy (A,B) and by SEM (C-F). (A) The incisor surfaces in control mice appeared smooth. (B) K14-Cre;Fgfr1fl/fl mice showed an irregular dimpled enamel surface and attrition at the tip (arrow). (C-F) SEM analysis of the incisor tooth surface (C,D) and their dissected surface (E,F). (C,E) The enamel surface in control mice was smooth and contained well-formed enamel prisms in dissected samples. (D,F) The tooth surfaces of K14-Cre;Fgfr1fl/fl mice were rough, and their enamel rods showed irregular formation. D, dentin; E, enamel.
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Figure 4. SEM analysis of K14-Cre;Fgfr1fl/+ (control) and K14-Cre;Fgfr1fl/fl maxillary molars. C and D represent enlarged areas of A and B, respectively. (A,C) The tooth surfaces appeared very smooth in the control mice. (B,D) The surfaces of K14-Cre;Fgfr1fl/fl teeth were rough.
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Journal of Dental Research, Vol. 87, No. 3,
238-243 (2008)
DOI: 10.1177/154405910808700307

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