Molecular mechanism of keloid progression
Project/Area Number |
17K11551
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Plastic surgery
|
Research Institution | Tohoku Medical and Pharmaceutical University (2018-2020) Teikyo University (2017) |
Principal Investigator |
Gonda Koichi 東北医科薬科大学, 医学部, 教授 (50254925)
|
Co-Investigator(Kenkyū-buntansha) |
山岡 尚世 帝京大学, 医学部, 講師 (10444085)
五来 克也 帝京大学, 医学部, 講師 (40524773)
青井 則之 帝京大学, 医学部, 講師 (70431872)
小室 裕造 帝京大学, 医学部, 教授 (90306928)
|
Project Period (FY) |
2017-04-01 – 2021-03-31
|
Project Status |
Completed (Fiscal Year 2020)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 創傷治癒 / 糖代謝 / ブドウ糖需要 / ケロイド / ブドウ糖 / 血糖 / 肥厚性瘢痕 / フィブロネクチン / EDA-FN / 選択的スプライシング |
Outline of Final Research Achievements |
We could not fully demonstrate the relevance of the aberrant expression of EDA-FN and its possible splicing abnormalities to the progression of keloid lesions, partly because we were not able to accept a substantial donation of keloid tissues and their derivative fibroblasts. During the course of this study, however, we have found out the unexpected association between the cellular glucose consumption and wound healing phenomenon (Cells autoregulate their gulucose demand according to the extracellular glucose supply). Based on this finding, we successfully recapitulate the autoregulatory phenomenon of glucose demand in a tissue level responding to the hematogenous glucose supply in 'in vivo' rodent model(Takeuchi K, Gonda K et al. Plast Reconstr Surg 144;409e, 2019). We are now further investigating the molecular mechanisms underlying this cellular autoregulation of glucose demand.
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Academic Significance and Societal Importance of the Research Achievements |
ブドウ糖の細胞内取り込みは、インスリン刺激や細胞内ATP量の減少に伴うAMPK(AMP-activated protein kinase)の活性化によって、細胞外ブドウ糖濃度の高低に反応してそれぞれ正や負の方向に調節される一方、それにも関わらず、細胞内では一定のブドウ糖消費が行われている、と暗黙の想定がなされている。ところが実際は、細胞レベルでも組織レベルでも、ブドウ糖の需要量の側も供給量の多寡によって調節が行われている、という事実が見出された。これは、高血糖・低血糖下の糖代謝、および、生物の飢餓に対する生存戦略の基本メカニズムに対するさらなる解明の糸口になると期待される。
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Report
(5 results)
Research Products
(15 results)