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Towards a standardized diabetic prolonged wound healing model in hairless SKH1 mice




TekijätKoivunotko, Elle; Monola, Julia; Pridgeon, Chris S.; Linden, Jere; Harjumäki, Riina; Yatkin, Emrah; Madetoja, Mari; Yliperttula, Marjo

Julkaisuvuosi2026

Lehti: Experimental Biology and Medicine

Artikkelin numero10857

Vuosikerta251

ISSN1535-3702

eISSN1535-3699

DOIhttps://doi.org/10.3389/ebm.2026.10857

Julkaisun avoimuus kirjaamishetkelläAvoimesti saatavilla

Julkaisukanavan avoimuus Kokonaan avoin julkaisukanava

Verkko-osoitehttps://doi.org/10.3389/ebm.2026.10857

Rinnakkaistallenteen osoitehttps://research.utu.fi/converis/portal/detail/Publication/522953314

Rinnakkaistallenteen lisenssiCC BY

Rinnakkaistallennetun julkaisun versioKustantajan versio


Tiivistelmä

Chronic wounds, particularly those associated with diabetes, pose a significant clinical challenge due to their impaired healing dynamics and lack of reliable and standardized preclinical models. This pilot study aimed to establish a diabetogenic, immunocompetent, hairless mouse model (SKH1 strain) to simulate prolonged wound healing. Diabetes was induced by streptozotocin administration, followed by the creation of full-thickness dorsal skin wounds. Wounds were treated with either saline or nanofibrillated cellulose hydrogel as a model treatment. Wound healing progression and blood glucose were monitored, and histopathological assessments were performed after a 14-day experiment. In addition, for the first time, the Thermidas thermal imaging system was used in an in vivo mouse model to evaluate skin temperature. Results demonstrated that diabetes induction successfully prolonged wound closure by 5 days compared with the previously described acute wound model in the same strain with the identical protocol without streptozotocin (STZ) induction. Histopathological analyses showed increased macrophage activity (16.2% vs. 2.2% in the treatment groups and 10.2% vs. 0.3% in the control groups) and decreased collagen deposition (12.2% vs. 43.2% in the treatment groups and 17.6% vs. 27.4% in the control groups), suggesting prolonged wound healing. These findings support the use of hairless SKH1 mice as a viable model for studying prolonged diabetic wound healing and evaluating future therapeutic candidates.


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Julkaisussa olevat rahoitustiedot
EK acknowledges the Post Docs in Companies program 2025 funded by Jenny and Antti Wihuri Foundation. JM acknowledges the Doctoral Programme in Materials Research and Nanosciences (University of Helsinki, Finland). CP acknowledges the Finnish Cultural Foundation (grant no. 00250755). RH and MY acknowledge the Academy of Finland, GeneCellNano flagship-project (grant no. 337430) and RH acknowledges the Finnish Cultural Foundation (grant no. 00220283).


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