Research for fibrous dysplasia using mutated GNAS1 transgenic mouse model

2014 Fiscal Year Final Research Report

• Project/Area Number: 24592763
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Morphological basic dentistry
• Research Institution: Osaka University
• Principal Investigator: SATO Sunao 大阪大学, 歯学研究科(研究院), 講師 (70335660)
• Co-Investigator(Kenkyū-buntansha): ABE Makoto 大阪大学, 大学院歯学研究科, 講師 (40448105) ; KISHINO Mitsunobu 大阪大学, 大学院歯学研究科, 助教 (60346161)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 線維性骨異形成症

Outline of Final Research Achievements

Fibrous dysplasia (FD) is common fibro-osseous lesions and activating point mutation of the alpha subunit of the stimulatory G protein gene (GNAS) causes FD. For FD patients, main medical treatment is surgical resection. Design of new effective ways of pharmacological intervention relies on appropriate FD animal model, however, to date there is no animal model suitable for reproduction of FD lesion. In this study, we produced cell line with GNAS point mutation and transgenic mice expressing GNAS point mutation with osteoblast specific. We examined the feature of these cell line and transgenic mice. Cell line with GNAS point mutation showed the similar gene expression with FD patients and transgenic mice had bone morphological change compared to wild type mice.
These results suggest that cell line with GNAS point mutation and transgenic mice with osteoblast specific GNAS point mutation are a useful FD model.

Free Research Field

口腔病理