| Project/Area Number |
18K19654
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Review Section |
Medium-sized Section 57:Oral science and related fields
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| Research Institution | Nagasaki University |
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Principal Investigator |
KOMORI Toshihisa 長崎大学, 医歯薬学総合研究科(歯学系), 教授 (00252677)
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| Project Period (FY) |
2018-06-29 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2019: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2018: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | I型コラーゲン / Runx2 / 骨粗鬆症 / 骨芽細胞 / Ｉ型コラーゲン / 転写 |
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| Outline of Final Research Achievements |
Type I collagen is a major organic substrate and composes more than 90% of bone. Type I collagen is composed of two α1 strands and one α2 strand forming a triple helical structure. Theα1 strand is encoded by Col1a1, and the α2 strand is encoded by Col1a2. 2.3 kb DNA upstream of the transcription start site has been shown to regulate Col1a1 expression in osteoblasts. However, it still remains to be clarified how Col1a1 expression is regulated. We found that Runx2, which is a master transcription factor for osteoblast differentiation, plays an important role in the regulation of Col1a1 expression in osteoblasts.
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| Academic Significance and Societal Importance of the Research Achievements |
骨粗鬆症は国内だけでも1280万人おり、高齢化に伴いその数は年々増加している。しかし、長期間使える骨形成促進剤は存在しない。I型コラーゲンは、骨の大部分を占める重要な基質タンパク質であり、その発現制御機構の解明は、骨粗鬆症の治療薬の開発や、骨再生療法の開発に非常に重要である。したがって、今回その発現制御機構の一端を明らかにしたことは、今後その全容解明につながり学術的に重要であるのはもちろんであるが、骨形成促進剤の開発にも大きく貢献する。
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