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Related Experiment Video

Updated: May 17, 2026

In Vitro Model of Human Cutaneous Hypertrophic Scarring using Macromolecular Crowding
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In Vitro Model of Human Cutaneous Hypertrophic Scarring using Macromolecular Crowding

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Development, validation and testing of a human tissue engineered hypertrophic scar model.

Leonarda J van den Broek1, Frank B Niessen, Rik J Scheper

  • 1Department Dermatology, VU University Medical Center, Amsterdam, the Netherlands.

ALTEX
|November 10, 2012
PubMed
Summary

A new tissue-engineered human hypertrophic scar (HTscar) model using adipose derived mesenchymal stem cells (ASC) offers a reliable, animal-free method for testing scar-reducing therapeutics.

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Area of Science:

  • Biomedical Engineering
  • Dermatology
  • Regenerative Medicine

Background:

  • Hypertrophic scars are a common complication of full-thickness skin wounds.
  • Existing animal and in vitro models for testing scar-reducing therapeutics are limited.
  • Adipose derived mesenchymal stem cells (ASC) play a role in scar formation.

Purpose of the Study:

  • To develop and validate a novel tissue-engineered human hypertrophic scar (HTscar) model.
  • To assess the utility of this model for testing anti-scar therapeutics.
  • To reduce reliance on animal models for scar research.

Main Methods:

  • Constructed a tissue-engineered HTscar model using reconstructed epidermis on a dermal matrix with ASC.
  • Quantified key HTscar parameters including contraction, dermal thickness, collagen-1, epidermal outgrowth, epidermal thickness, and cytokine secretion (IL-6, CXCL8).

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Last Updated: May 17, 2026

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A Mouse Model of Mechanotransduction-driven, Human-like Hypertrophic Scarring
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Visualizing Scar Development Using SCAD Assay - An Ex-situ Skin Scarring Assay
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  • Validated the model using established scar treatments (5-fluorouracil, triamcinolone), an ineffective agent (1,25-dihydroxyvitamin-D3), and potential novel agents (atorvastatin, retinoic acid).
  • Main Results:

    • The ASC-containing model successfully facilitated HTscar formation.
    • The model demonstrated sensitivity to known scar therapeutics and identified atorvastatin as a potential treatment.
    • Different therapeutics selectively impacted various scar parameters, suggesting potential for combination therapies.

    Conclusions:

    • The developed animal-free HTscar model is a viable tool for mechanistic studies and in vitro testing of anti-scar therapeutics.
    • This model can aid in the discovery of novel scar treatments and reduce animal testing.
    • Atorvastatin shows promise as a potential therapeutic for hypertrophic scar reduction.