periostin Null Mice Exhibit Dwarfism, Incisor Enamel Defects, and an Early-Onset Periodontal Disease-Like Phenotype
| Autor: | Rhonda Rogers, Hong-Ming Zhou, Zhi Chen, Hector F. Rios, Simon J. Conway, Jian Wang, Agnieszka Kruzynska-Frejtag, Manabu Maeda, Jian Q. Feng, Shrinagesh V. Koushik, Andrew Lindsley, Haiyan Wang |
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| Rok vydání: | 2005 |
| Předmět: |
Male
Pathology medicine.medical_specialty Dwarfism Biology Periostin Bone and Bones Mice Genes Reporter Mammalian Genetic Models with Minimal or Complex Phenotypes medicine Animals Periodontal fiber Dental Enamel Molecular Biology Periodontal Diseases Bone growth Periosteum Enamel paint Soft diet Cell Biology Amelogenesis Anatomy beta-Galactosidase Mice Mutant Strains Incisor Phenotype medicine.anatomical_structure visual_art Ameloblast differentiation visual_art.visual_art_medium Female Cell Adhesion Molecules Infertility Female |
| Zdroj: | Molecular and Cellular Biology. 25:11131-11144 |
| ISSN: | 1098-5549 |
| Popis: | Periostin was originally identified as an osteoblast-specific factor and is highly expressed in the embryonic periosteum, cardiac valves, placenta, and periodontal ligament as well as in many adult cancerous tissues. To investigate its role during development, we generated mice that lack the periostin gene and replaced the translation start site and first exon with a lacZ reporter gene. Surprisingly, although periostin is widely expressed in many developing organs, periostin-deficient (peri(lacZ)) embryos are grossly normal. Postnatally, however, approximately 14% of the nulls die before weaning and all of the remaining peri(lacZ) nulls are severely growth retarded. Skeletal analysis revealed that trabecular bone in adult homozygous skeletons was sparse, but overall bone growth was unaffected. Furthermore, by 3 months, the nulls develop an early-onset periodontal disease-like phenotype. Unexpectedly, these mice also show a severe incisor enamel defect, although there is no apparent change in ameloblast differentiation. Significantly, placing the peri(lacZ) nulls on a soft diet that alleviated mechanical strain on the periodontal ligament resulted in a partial rescue of both the enamel and periodontal disease-like phenotypes. Combined, these data suggest that a healthy periodontal ligament is required for normal amelogenesis and that periostin is critically required for maintenance of the integrity of the periodontal ligament in response to mechanical stresses. |
| Databáze: | OpenAIRE |
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