2017 Fiscal Year Final Research Report
The Role of Shh in developing fetal mouse submandibular gland.
| Project/Area Number |
15K11281
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Surgical dentistry
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| Research Institution | Asahi University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
水越 堅詞 朝日大学, 歯学部, 助教 (90631565)
佐藤 慶太郎 朝日大学, 歯学部, 講師 (10549041)
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| Research Collaborator |
KASHIMATA Masanori
GRESIK Edward
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | 顎下腺 / 分枝形態形成 / 上皮間葉相互作用 / Shh/Ptch / EGF/ErbB |
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| Outline of Final Research Achievements |
The fundamental processes of epithelio-mesenchymal interactions depend both on a variety of growth factors and their receptors. Shh are well known as a morphogen that plays many important roles during development of numerous organs. In this study, we investigated the relationship between Shh/Ptch and EGF/ErbB signals of developing fetal mouse SMG. Shh stimulated BrM and induced phosphorylations of ErbB1 and ERK1/2 in SMG rudiments. Shh also significantly induced mRNA syntheses for EGF ligand and ErbB family. Induction of mRNA level of Egf was specific in mesenchyme and inductions of mRNA levels for Erbb1, Erbb2 and Erbb3 were specific in epithelium of SMG rudiments. Gli1 transcription factor level was elevated by administrations of Shh to cultured SMG rudiments. These results suggested that Shh stimulates BrM of fetal mouse SMG through an activation of EGF/ErbB/ERK1/2 signaling systems, and the stimulations by Shh may be regulated by the transcription factor, Gli1.
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| Free Research Field |
歯科薬理学分野
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