Hepatocyte growth factor reverses the TGF-beta-induced growth inhibition of CCL-64 cells. A novel bioassay for HGF and implications for the TGF-beta bioassay

J Immunol Methods. 1996 Jan 16;189(1):59-64. doi: 10.1016/0022-1759(95)00228-6.

Abstract

The influence of human hepatocyte growth factor (HGF) on the transforming growth factor beta (TGF-beta) bioassay CCL-64 was examined. HGF induced proliferation of the CCL-64 cells and potently counteracted TGF-beta-induced growth inhibition. HGF was not inactivated by transient acidification to pH 2, a commonly used procedure to activate latent TGF-beta. HGF was a stronger mitogen for the mink lung cells than epidermal growth factor (EGF), a known stimulator of CCL-64 cell growth. Costimulation of the cells by these two cytokines resulted in an additive effect on proliferation. In complex biological fluids containing large amounts of HGF, the TGF-beta concentration can be underestimated when determined by the CCL-64 assay. When a fixed amount of TGF-beta is added, the CCL-64 cells can be used as a reliable bioassay for HGF with a sensitivity of about 1 ng/ml.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bronchoalveolar Lavage Fluid / chemistry
  • Cell Division / drug effects
  • Cell Line
  • Epidermal Growth Factor / pharmacology
  • Growth Inhibitors / antagonists & inhibitors*
  • Growth Inhibitors / pharmacology
  • Hepatocyte Growth Factor / analysis
  • Hepatocyte Growth Factor / pharmacology*
  • Humans
  • Lung / cytology
  • Lung / drug effects
  • Mice
  • Mink
  • Multiple Myeloma / metabolism
  • Transforming Growth Factor beta / antagonists & inhibitors*
  • Transforming Growth Factor beta / pharmacology

Substances

  • Growth Inhibitors
  • Transforming Growth Factor beta
  • Epidermal Growth Factor
  • Hepatocyte Growth Factor