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Int. J. Mol. Sci. 2017, 18(2), 438; doi:10.3390/ijms18020438

Effects of Remote Ischemic Preconditioning on Heme Oxygenase-1 Expression and Cutaneous Wound Repair

1
Department of Orthodontics and Craniofacial Biology, Radboud University Medical Center, Nijmegen 6500HB, The Netherlands
2
Department of Rheumatology, Radboud University Medical Center, Nijmegen 6500HB, The Netherlands
3
Central Animal Laboratory, Radboud University Medical Center, Nijmegen 6500HB, The Netherlands
4
Radboud Institute for Molecular Life Sciences, Nijmegen 6500HB, The Netherlands
5
Radboud Institute for Health Sciences, Nijmegen 6500HB, The Netherlands
6
Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305, USA
7
Department of Surgery, University Medical Center Groningen, Groningen 9700RB, The Netherlands
8
Department of Human Genetics, Radboud University Medical Center, Nijmegen 6500HB, The Netherlands
9
Department of Oral Health Sciences, Faculty of Medicine, KU Leuven, 3000 Leuven, Belgium
*
Author to whom correspondence should be addressed.
Academic Editor: Allison Cowin
Received: 20 December 2016 / Revised: 6 February 2017 / Accepted: 13 February 2017 / Published: 17 February 2017
(This article belongs to the Special Issue Wound Repair and Regeneration)
View Full-Text   |   Download PDF [4840 KB, uploaded 17 February 2017]   |  

Abstract

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. View Full-Text
Keywords: remote ischemic preconditioning; heme oxygenase-1; tissue injury; wound repair remote ischemic preconditioning; heme oxygenase-1; tissue injury; wound repair
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MDPI and ACS Style

Cremers, N.A.J.; Wever, K.E.; Wong, R.J.; van Rheden, R.E.M.; Vermeij, E.A.; van Dam, G.M.; Carels, C.E.; Lundvig, D.M.S.; Wagener, F.A.D.T.G. Effects of Remote Ischemic Preconditioning on Heme Oxygenase-1 Expression and Cutaneous Wound Repair. Int. J. Mol. Sci. 2017, 18, 438.

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