2025/09/30 更新

写真a

マツナガ ノリコ
松永 宜子
matsunaga noriko
所属
武蔵小杉病院 形成外科 助教
職名
助教
外部リンク

論文

  • Toe Keloids Treated with Core Excision, Postoperative Radiotherapy, and Steroid Plaster. 国際誌

    Chiemi Kaku, Noriko Matsunaga, Shigehiko Kuribayashi, Rei Ogawa

    Plastic and reconstructive surgery. Global open   8 ( 9 )   e3085   2020年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Although keloids are common on the joints, precordial areas, and abdomen, toe keloids are rare. The limited literature to date also suggests that they can be difficult to treat. We experienced the case of a 21-year-old woman with toe keloids on the first, second, and third toes that arose after ingrown-nail operations at another hospital. The second toe keloid was resected but recurred. Since subsequent conservative treatments were ineffective, the patient was referred to our hospital. The first visit revealed three large keloids: in particular, the keloid on the second toe had engulfed the entire circumference of the toe. Surgery with the core-excision method and postoperative radiotherapy were performed. After the sutures were removed, the scars were treated for 24 hours/day with steroid plaster until the induration disappeared. One and a half years after the operation, recurrence was not observed and the appearance of the toes had improved greatly. Thus, combination therapy composed of core excision, radiotherapy, and steroid plaster therapy is highly effective for toe keloids.

    DOI: 10.1097/GOX.0000000000003085

    PubMed

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  • The Immunosuppressant Fingolimod (FTY720) for the Treatment of Mechanical Force-Induced Abnormal Scars. 国際誌

    Masayo Aoki, Akatsuki Kondo, Noriko Matsunaga, Azusa Honda, Yuri Okubo, Kazuaki Takabe, Rei Ogawa

    Journal of immunology research   2020   7057195 - 7057195   2020年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    AIM: Abnormal scars such as hypertrophic scars (HSs) and keloids are excessively growing scars that exhibit chronic inflammation and capillary vasculogenesis. The lipid mediator sphingosine-1-phosphate (S1P) is important in inflammatory cell recruitment and angiogenesis. Fingolimod (FTY720) is an analog of S1P and thus functionally antagonizes S1P receptors and inhibits the enzyme that produces S1P. We examined the effects of topical FTY720 injections on mechanical force-induced HS progression. METHODS: Mechanical force-induced HSs were generated in C57BL6/J mice by suturing a dorsal incision and applying a stretching device on Days 6, 8, 10, and 12. On Days 8, 10, and 12, intracutaneous FTY720 (10 μM) or control vehicle injections were performed. On Day 14, scar tissues and blood were procured and subjected to histology and flow cytometry. RESULTS: Flow cytometry showed that FTY720 decreased the frequencies of macrophages with M2 predominance in the scars but had no effect on total, CD4+, or CD8a+ T cell frequencies. FTY720 also decreased the vascular endothelial cell frequencies in the scar along with the microvessels, as determined by immunohistochemistry. Compared to the vehicles, FTY720 treatment significantly reduced the gross scar area and the cross-sectional scar area on histology. On the other hand, FTY720 tended to reduce white blood cells and significantly reduced the lymphocyte frequencies in the blood. CONCLUSION: Topical FTY720 induces M2 predominance and impairs angiogenesis. Therefore, its local immunosuppressive mechanisms differ from those of conventional immunosuppressive agents. Topical FTY720 can be a novel therapeutic option for abnormal scars that are difficult to control with corticosteroids. Its lymphocytopenic effects may be limited by careful optimization of the treatment regimen.

    DOI: 10.1155/2020/7057195

    PubMed

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共同研究・競争的資金等の研究課題

  • ヒト皮膚線維芽細胞に対する圧刺激の感知機構の解明

    研究課題/領域番号:20K18424  2020年4月 - 2025年3月

    日本学術振興会  科学研究費助成事業  若手研究

    松永 宜子

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    配分額:3120000円 ( 直接経費:2400000円 、 間接経費:720000円 )

    伸展刺激や圧刺激がコラーゲン産生や血管新生を誘導して創傷治癒を加速する治療方法を開発した先行研究を参考に、本研究では、自ら産生した細胞外基質に取り囲まれアクチンに富んだ線維芽細胞において、細胞頂上面からの力学的刺激依存的な細胞の増殖・分化の制御機構を解明し、生体の恒常性維持機構を調べる。種々の炎症メディエーターとして、皮膚の過度な周期的伸展を負荷する物理的刺激、および、アレルギー反応や炎症の発現を介在するヒスタミンやATPなどの薬剤刺激にフォーカスし、NHDF細胞の種々の刺激に対する細胞変形や遊走・運動などの細胞動態や、刺激に伴う上流の応答として細胞内Ca2+動員や細胞外K+放出が生じると考え、実験を繰り返した。例えば、過度な伸展刺激の実験では、I型コラーゲンコートした伸展可能なシリコーン製チャンバーに正常ヒト皮膚線維芽細胞(NHDF)を播種した後、伸展率20%で5秒おきに1秒間30回の伸展を繰り返して炎症時を模し、細胞動態を顕微鏡で観察した。その結果、細胞形態として著しく急激な細胞の収縮が観察された。一方、最近インフラマソーム(炎症反応を惹起するための細胞内タンパク質複合体)の阻害剤として注目されているβ-ヒドロキシ酪酸(25 mM)を測定開始10分前にあらかじめ共存させて同様に伸展を繰り返しても、顕著な細胞収縮は少なからず観察された。すなわち、過度な伸展刺激による持続的な細胞の形態変化の抑制はβ-ヒドロキシ酪酸では十分抑制されなかった。炎症因子をヒスタミンやATPにした場合、β-ヒドロキシ酪酸 (25 mM)で抑制された。薬剤因子と機械刺激因子で炎症メカニズムが異なっていることが分かりつつある。

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