Low-energy extracorporeal shock wave therapy enhances skin wound healing in diabetic mice: A critical role of endothelial nitric oxide synthase.

Low-energy extracorporeal shock wave ( LE- ESW) treatment has been shown to accelerate wound repair; however, the mechanisms of treatment remain unclear. In the present study, we addressed the role of endothelial nitric oxide synthase ( eNOS). A single LE- ESW treatment accelerated the healing of wo...

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Publicado en:Wound Repair & Regeneration Vol. 20; no. 6; pp. 887 - 896
Autores principales: Hayashi, Denso, Kawakami, Kazuyoshi, Ito, Kenta, Ishii, Keiko, Tanno, Hiromasa, Imai, Yoshimichi, Kanno, Emi, Maruyama, Ryoko, Shimokawa, Hiroaki, Tachi, Masahiro
Formato: pictorial research tables/charts Journal Article
Publicado: Wiley-Blackwell Nov/Dec2012
Acceso en línea:Ver este registro en EBSCOhost
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        10.1111/j.1524-475X.2012.00851.x
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        atl: Low-energy extracorporeal shock wave therapy enhances skin wound healing in diabetic mice: A critical role of endothelial nitric oxide synthase.
      aug:
        au:
          Hayashi, Denso
          Kawakami, Kazuyoshi
          Ito, Kenta
          Ishii, Keiko
          Tanno, Hiromasa
          Imai, Yoshimichi
          Kanno, Emi
          Maruyama, Ryoko
          Shimokawa, Hiroaki
          Tachi, Masahiro
        affil: Department of Plastic and Reconstructive Surgery, Tohoku University Graduate School of Medicine
      sug:
        subj:
          Lithotripsy
          Wound Healing
          Skin
          Diabetes Mellitus
          Endothelium Physiology
          Enzymes
          Nitric Oxide Metabolism
          Animal Studies
          Mice
          Models, Biological
          Funding Source
          Growth Substances
          Immunohistochemistry
          Blotting, Western
          Reverse Transcriptase Polymerase Chain Reaction
          Descriptive Statistics
          T-Tests
          Data Analysis Software
      ab: Low-energy extracorporeal shock wave ( LE- ESW) treatment has been shown to accelerate wound repair; however, the mechanisms of treatment remain unclear. In the present study, we addressed the role of endothelial nitric oxide synthase ( eNOS). A single LE- ESW treatment accelerated the healing of wounds in diabetic mice caused by the injection of streptozotocin. This accelerated healing was accompanied by the increased expression of eNOS and vascular endothelial growth factor ( VEGF) and the generation of new vessels at the wound tissues. These results raised the possibility that eNOS may be involved in the beneficial effects of LE- ESW treatment. To address this possibility, we compared the effects of this treatment between mice with a genetic disruption of eNOS knockout ( eNOS-KO mice) and wild-type ( WT) control mice. Interestingly, the LE- ESW-induced acceleration of wound closure and the increase in VEGF expression and neovascularization was significantly attenuated in eNOS-KO mice compared with WT mice. Considered collectively, these results showed that eNOS was induced at the wound tissues by LE- ESW treatment and played a critical role in the therapeutic effects of this treatment by accelerating the wound healing by promoting VEGF expression and neovascularization.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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