Identification, culture, and characterization of pancreatic stellate cells in rats and humans

Gastroenterology. 1998 Aug;115(2):421-32. doi: 10.1016/s0016-5085(98)70209-4.


Background & aims: Until now, the basic matrix-producing cell type responsible for pancreas fibrosis has not been identified. In this report, retinoid-containing pancreatic stellate cells (PSCs) in rat and human pancreas are described, and morphological and biochemical similarities to hepatic stellate cells are shown.

Methods: Electron and immunofluorescence microscopy (collagen types I and III, fibronectin, laminin, alpha-actin, and desmin) was performed using pancreatic tissue and cultured PSCs. Extracellular matrix synthesis was shown using quantitative immunoassay and Northern blot analysis.

Results: PSCs are located in interlobular areas and in interacinar regions. Early primary cultured PSCs contain retinol and fatty acid retinyl-esters. Addition of retinol to passaged cells resulted in retinol uptake and esterification. During primary culture, the cells changed from a quiescent fat-storing phenotype to a highly synthetic myofibroblast-like cell expressing iso-alpha-smooth muscle actin (>90%) and desmin (20%-40%) and showing strong positive staining with antibodies to collagen types I and III, fibronectin, and laminin. As determined on protein and messenger RNA level, serum growth factors stimulated the synthesis of collagen type I and fibronectin.

Conclusions: The identification of PSCs, particularly in fibrotic areas, and the similarities of these cells to hepatic stellate cells suggest that PSCs participate in the development of pancreas fibrosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Separation
  • Cells, Cultured
  • Collagen / metabolism
  • Fibronectins / metabolism
  • Fibrosis
  • Fluorescent Antibody Technique
  • Humans
  • Laminin / metabolism
  • Male
  • Pancreas / metabolism
  • Pancreas / pathology*
  • Rats
  • Rats, Wistar
  • Reference Values
  • Retinoids / metabolism


  • Fibronectins
  • Laminin
  • Retinoids
  • Collagen