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Related Experiment Video

Updated: Jun 11, 2025

Protocol to Create Chronic Wounds in Diabetic Mice
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Dysregulated S100A9 Expression Impairs Matrix Deposition in Chronic Wounds.

Sandra Franz1, Marta Torregrossa1, Ulf Anderegg1

  • 1Department of Dermatology, Venereology and Allergology, Max Bürger Research Centre, Medical Faculty, University Leipzig, Johannisallee 30, 04103 Leipzig, Germany.

International Journal of Molecular Sciences
|September 28, 2024
PubMed
Summary

Overexpressed S100A9 protein impairs extracellular matrix (ECM) deposition in chronic wounds. Blocking S100A9 in diabetic wound models restored ECM functions, suggesting S100A9 as a therapeutic target for chronic wound healing.

Keywords:
S100A8S100A9chronic woundsdiabetesextracellular matrixfibroblastsiron overload

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Area of Science:

  • Biomedical Science
  • Wound Healing Research
  • Molecular Biology

Background:

  • Chronic non-healing wounds exhibit persistent inflammation and impaired extracellular matrix (ECM) synthesis.
  • S100A8/A9 proteins are dysregulated in delayed wound healing, affecting immune cell function.

Purpose of the Study:

  • To investigate the pathological role of S100A9 overexpression in fibroblast ECM function in impaired wound healing models.
  • To explore S100A9 as a potential therapeutic target for chronic wound treatment.

Main Methods:

  • Utilized db/db mice (diabetes model) and iron-overloaded mice (chronic venous leg ulcer model).
  • Analyzed S100A8/A9 expression, ECM deposition, and inflammatory mediators in wound tissues.
  • Investigated the mechanism of S100A9 action on fibroblast ECM functions via toll-like-receptor 4 (TLR4) signaling.
  • Assessed the therapeutic effect of blocking S100A9 in db/db mouse wounds.

Main Results:

  • Both mouse models showed delayed wound closure, sustained inflammation, and decreased ECM deposition, mirroring human chronic wounds.
  • Prolonged S100A8 and S100A9 expression correlated with compromised ECM deposition in these models and in human chronic wounds.
  • S100A9 was found to directly alter fibroblast ECM protein and enzyme expression via TLR4-dependent signaling.
  • Blocking S100A9 in db/db mice restored fibroblast ECM functions and increased matrix deposition.

Conclusions:

  • Dysregulated S100A9 directly contributes to compromised ECM deposition in chronic wounds.
  • S100A9 plays an unrecognized pathological role in affecting fibroblast ECM functions.
  • S100A9 represents a promising therapeutic target for enhancing tissue repair in chronic wounds.