Induction of fibronectin gene expression by inhibitors of protein phosphatase type 2B in normal and transformed fibroblasts

Exp Mol Med. 1999 Jun 30;31(2):71-5. doi: 10.1038/emm.1999.12.

Abstract

Two intracellular signal pathways mediated by cAMP and protein kinase C (PKC) were involved in the regulation of FN gene expression (Lee et al., Exp. Mol. Med. 30: 240, 1998). In this study, a possible involvement of protein phosphatase-dependent pathways in the regulation of FN gene expression was investigated by using protein phosphatase type 2B (PP2B) inhibitors, cyclosporin A and ascomycin. Both cyclosporin A and ascomycin increased the levels of FN mRNA in WI-38 human lung fibroblasts and the SV40-transformed WI-38 cells but not in MC3T3-E1 osteoblasts. The expression of FN appears to increase from six hours up to 48 hours after treatment suggesting that it is not an immediate effect. In addition, this effect required a new protein synthesis. Neither cyclosporin A nor ascomycin affects the phorbol myristate acetate (PMA)-induced stimulation of FN gene expression and the same result occurred in vice versa suggesting the mechanism of PMA and cyclosporin A/ascomycin in the regulation of FN gene expression may share a common downstream pathway. Taken together, this study suggests that PP2B is involved in the regulation of FN gene expression in normal and transformed fibroblasts but not in osteoblasts.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcineurin Inhibitors*
  • Cell Line, Transformed
  • Cell Transformation, Viral
  • Cyclosporine / pharmacology*
  • Enzyme Inhibitors / pharmacology
  • Fibroblasts
  • Fibronectins / genetics*
  • Fibronectins / metabolism
  • Gene Expression Regulation*
  • Humans
  • Lung / cytology
  • Mice
  • Osteoblasts
  • Tacrolimus / analogs & derivatives*
  • Tacrolimus / pharmacology

Substances

  • Calcineurin Inhibitors
  • Enzyme Inhibitors
  • Fibronectins
  • Cyclosporine
  • immunomycin
  • Tacrolimus