Inhibition of insulin-like growth factor-I mitogenic action by zinc chelation is associated with a decreased mitogen-activated protein kinase activation in RAT-1 fibroblasts

FEBS Lett. 1999 Apr 23;449(2-3):284-8. doi: 10.1016/s0014-5793(99)00419-6.

Abstract

The mechanisms responsible for the resistance to the anabolic actions of IGF-I induced by zinc deficiency are not understood. We showed that zinc chelation by DTPA (diethylenetriaminepenta-acetic acid) inhibits [3H]thymidine incorporation stimulated by IGF-I in Rat-1 fibroblasts. This inhibition was specific of zinc chelation since it was prevented by the addition of zinc to DTPA. The stimulation of MAPK, which is crucial for the [3H]thymidine incorporation induced by IGF-I in Rat-1 cells, was partially blunted by DTPA. Therefore, the inhibition of the mitogenic action of IGF-I in Rat-1 fibroblasts by DTPA is potentially caused by decreased MAPK activation by IGF-I.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium-Calmodulin-Dependent Protein Kinases / metabolism*
  • Cell Division
  • Cell Line
  • Chelating Agents / pharmacology
  • Enzyme Activation
  • Fibroblasts / drug effects
  • Fibroblasts / metabolism
  • Insulin-Like Growth Factor I / antagonists & inhibitors
  • Insulin-Like Growth Factor I / metabolism*
  • Isotope Labeling
  • Pentetic Acid / pharmacology
  • Rats
  • Tritium
  • Zinc / metabolism*

Substances

  • Chelating Agents
  • Tritium
  • Insulin-Like Growth Factor I
  • Pentetic Acid
  • Calcium-Calmodulin-Dependent Protein Kinases
  • Zinc