Overview

Evidence shows that fibrosis is a result of misregulated complex pathways involving multiple cell types, such as epithelial cells and fibroblasts. Charles River has optimized an off-the-shelf panel of in vitro assays using patient-derived primary cells to measure the transdifferentiation of epithelial cells and fibroblasts as a translational tool for drug therapies:

  • Epithelial-to-mesenchymal (EMT) assay: Primary human bronchial fibroblasts derived from idiopathic pulmonary fibrosis (IPF) patients and healthy donors are stimulated with TGF-β1. The transdifferentiation of epithelial cells into motile mesenchymal cells is measured with biomarker fibronectin (FN1) via high-content imaging.
  • Fibroblasts-to-myofibroblasts (FMT) assay: Primary human bronchial fibroblasts derived from IPF patients and healthy donors are stimulated with TGF-β1. The transdifferentiation of fibroblasts-to-myofibroblasts is measured with biomarker alpha-smooth muscle actin (αSMA) via high-content imaging.

View our poster to see a comparison of compounds with claimed anti-fibrotic activity in two novel human primary cell-based assays using IPF-derived patient material.

For your scheduling convenience, EMT and FMT assays are routinely run on a bimonthly basis. Refer to our technical sheets for assay details and schedules:

Additional fibrosis capabilities we offer include:

  • Macrophage differentiation – M1/M2
  • Fibroblast migration – scratch assay; wound closure
  • Epithelial migration – scratch assay; wound closure
  • Fibroblast gel contractility
  • Fibroblast impedance – contractility
  • Hepatic stellate cell to myofibroblast transition