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Interleukins decrease epithelial protein and gene expression by K14 + CD105+ equine hoof progenitor cells.

Qingqiu Yang1, Mandi J Lopez2,3

  • 1Laboratory for Equine & Comparative Orthopedic Research, Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA, USA.

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|April 16, 2026
PubMed
Summary
This summary is machine-generated.

Inflammatory interleukins promote mesenchymal transition in equine hoof progenitor cells, while the natural matrix supports epidermal healing. This research offers insights into progenitor cell behavior for improved hoof tissue repair.

Keywords:
EctodermEpithelial-mesenchymal transitionFingernailHorseLaminitisMatricalStem cell

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Area of Science:

  • Equine hoof biology
  • Progenitor cell research
  • Wound healing mechanisms

Background:

  • Epithelial to mesenchymal transition (EMT) of progenitor cells in the equine hoof's stratum internum (SI) may affect healing.
  • K14+CD105+ equine hoof SI progenitor cells were investigated for their potential to adopt a mesenchymal phenotype when exposed to inflammatory interleukins in vitro.

Purpose of the Study:

  • To investigate the role of K14+CD105+ progenitor cells in equine hoof healing.
  • To determine if inflammatory interleukins induce mesenchymal transition in these cells.
  • To explore the influence of the native matrix on cell differentiation.

Main Methods:

  • Quantified K14+CD105+ progenitor cells from healthy and scarred SI.
  • Prepared decellularized matrix from healthy SI.
  • Analyzed gene expression (e.g., E-cadherin, N-cadherin, TGF-β) and cell phenotypes in vitro under various conditions (stromal medium, IL medium, on matrix).

Main Results:

  • K14+CD105+ progenitor cells maintained their immunophenotype in vitro.
  • Inflammatory interleukins (IL) promoted mesenchymal markers (e.g., N-cadherin, TGF-β3), while the matrix favored epidermal markers (e.g., E-cadherin, K10).
  • Differential gene expression of TGF-β and β-catenin was observed based on culture conditions.

Conclusions:

  • Inflammatory interleukins drive mesenchymal differentiation, whereas the healthy SI matrix supports epidermal differentiation.
  • K14+CD105+ progenitor cells from the SI niche are a valuable model for studying EMT and restoring tissue healing.
  • Findings have implications for equine hoof injury and disease treatment strategies.