| Autor: |
Cremers NA; Department of Orthodontics and Craniofacial Biology, Radboud University Medical Center, Nijmegen 6500HB, The Netherlands. niels.cremers@radboudumc.nl.; Department of Rheumatology, Radboud University Medical Center, Nijmegen 6500HB, The Netherlands. niels.cremers@radboudumc.nl.; Radboud Institute for Molecular Life Sciences, Nijmegen 6500HB, The Netherlands. niels.cremers@radboudumc.nl., Wever KE; Central Animal Laboratory, Radboud University Medical Center, Nijmegen 6500HB, The Netherlands. kim.wever@radboudumc.nl.; Radboud Institute for Health Sciences, Nijmegen 6500HB, The Netherlands. kim.wever@radboudumc.nl., Wong RJ; Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305, USA. rjwong@stanford.edu., van Rheden RE; Department of Orthodontics and Craniofacial Biology, Radboud University Medical Center, Nijmegen 6500HB, The Netherlands. rene.vanrheden@radboudumc.nl.; Radboud Institute for Molecular Life Sciences, Nijmegen 6500HB, The Netherlands. rene.vanrheden@radboudumc.nl., Vermeij EA; Department of Rheumatology, Radboud University Medical Center, Nijmegen 6500HB, The Netherlands. eline.vermeij@radboudumc.nl.; Radboud Institute for Molecular Life Sciences, Nijmegen 6500HB, The Netherlands. eline.vermeij@radboudumc.nl., van Dam GM; Department of Surgery, University Medical Center Groningen, Groningen 9700RB, The Netherlands. g.m.van.dam@umcg.nl., Carels CE; Department of Orthodontics and Craniofacial Biology, Radboud University Medical Center, Nijmegen 6500HB, The Netherlands. carine.carels@radboudumc.nl.; Radboud Institute for Molecular Life Sciences, Nijmegen 6500HB, The Netherlands. carine.carels@radboudumc.nl.; Department of Human Genetics, Radboud University Medical Center, Nijmegen 6500HB, The Netherlands. carine.carels@radboudumc.nl.; Department of Oral Health Sciences, Faculty of Medicine, KU Leuven, 3000 Leuven, Belgium. carine.carels@radboudumc.nl., Lundvig DM; Department of Orthodontics and Craniofacial Biology, Radboud University Medical Center, Nijmegen 6500HB, The Netherlands. dittelundvig@hotmail.com.; Radboud Institute for Molecular Life Sciences, Nijmegen 6500HB, The Netherlands. dittelundvig@hotmail.com., Wagener FA; Department of Orthodontics and Craniofacial Biology, Radboud University Medical Center, Nijmegen 6500HB, The Netherlands. frank.wagener@radboudumc.nl.; Radboud Institute for Molecular Life Sciences, Nijmegen 6500HB, The Netherlands. frank.wagener@radboudumc.nl. |
| Abstrakt: |
Skin wounds may lead to scar formation and impaired functionality. Remote ischemic preconditioning (RIPC) can induce the anti-inflammatory enzyme heme oxygenase-1 (HO-1) and protect against tissue injury. We aim to improve cutaneous wound repair by RIPC treatment via induction of HO-1. RIPC was applied to HO-1- luc transgenic mice and HO-1 promoter activity and mRNA expression in skin and several other organs were determined in real-time. In parallel, RIPC was applied directly or 24h prior to excisional wounding in mice to investigate the early and late protective effects of RIPC on cutaneous wound repair, respectively. HO-1 promoter activity was significantly induced on the dorsal side and locally in the kidneys following RIPC treatment. Next, we investigated the origin of this RIPC-induced HO-1 promoter activity and demonstrated increased mRNA in the ligated muscle, heart and kidneys, but not in the skin. RIPC did not change HO-1 mRNA and protein levels in the wound 7 days after cutaneous injury. Both early and late RIPC did not accelerate wound closure nor affect collagen deposition. RIPC induces HO-1 expression in several organs, but not the skin, and did not improve excisional wound repair, suggesting that the skin is insensitive to RIPC-mediated protection. |
