| Project/Area Number |
20K17340
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 53050:Dermatology-related
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| Research Institution | Gunma University |
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Principal Investigator |
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| Project Period (FY) |
2020-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2021: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2020: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 転写因子 / SOX2 / 皮膚虚血再灌流障害 / 急性期褥瘡 / 酸化ストレス |
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| Outline of Research at the Start |
本研究は皮膚に生じる床ずれ（褥瘡）に対する研究です。今回、私たちは遺伝子発現を制御する転写因子の1つであるSOX2に着目して検討を行います。皮膚組織に発現させたSOX2が褥瘡発症の際に生じる酸化ストレスをどのように制御するかを解明することを目的としています。今回の研究により褥瘡に対する新しい治療開発が期待されます。
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| Outline of Final Research Achievements |
The objective was to evaluate the role of transcription factor SOX2 in cutaneous ischemia-reperfusion(I/R) injury and the possible protective effect of SOX2 induction in keratinocytes on pressure ulcer formation in cutaneous I/R injury. Cutaneous I/R injury experiment was performed using wild type mouse and epidermal-specific SOX2 overexpressing mouse. Immunostaining and qPCR analysis showed that SOX2 expression is transiently expressed in the epidermis after cutaneous I/R injury. The development of ulcer formation was significantly inhibited in epidermal specific SOX2-overexpresing mice. Immunostaining using skin tissue at I/R site revealed that the number of infiltrating inflammatory cells, apoptotic cells, vascular damage, hypoxic areas were significantly suppressed in SOX2-overexpresing mice. qPCR assay revealed mRNA levels of inflammatory cytokines expression tended to be reduced in SOX2-overexpresing mice.
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| Academic Significance and Societal Importance of the Research Achievements |
本邦では今後も高齢化が進み褥瘡の発症リスクは増加の一途を辿ると考えられる。本研究成果によって、これまで発症予防に確立した治療がなかった急性期褥瘡において潰瘍形成を防ぐ新たな治療を開発することが出来れば難治性の褥瘡を発症する患者数や医療費の減少が期待できる可能性がある。
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