Stable transfection of calbindin-D28k into the GH3 cell line alters calcium currents and intracellular calcium homeostasis

Neuron. 1992 Nov;9(5):943-54. doi: 10.1016/0896-6273(92)90246-a.

Abstract

Previous work demonstrating the presence and differential distribution of Ca(2+)-binding proteins in the CNS has led to the proposal that cytosolic proteins, such as calbindin-D28k (CB), may play a pivotal role in neurons. We have used a retrovirus containing the full-length cDNA for CB to transfect the pituitary tumor cell line GH3, to generate CB-expressing GH3 cells and to investigate whether ionic channel activities as well as the concentration of intracellular free Ca2+ ([Ca2+]i) homeostasis could be altered by the presence of this Ca(2+)-binding protein. We show that CB-transfected GH3 cells exhibited lower Ca2+ entry through voltage-dependent Ca2+ channels and were better able to reduce [Ca2+]i transients evoked by voltage depolarizations than the wild-type parent cell line. These observations provide a mechanism by which CB may protect tissues against Ca(2+)-mediated excitotoxicity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calbindin 1
  • Calbindins
  • Calcium / metabolism*
  • Calcium Channels / physiology*
  • Cell Membrane / physiology
  • Chelating Agents / pharmacology
  • Electric Conductivity
  • Gene Expression
  • Genetic Vectors
  • Homeostasis / physiology*
  • Pituitary Neoplasms
  • Rats
  • Retroviridae / genetics
  • S100 Calcium Binding Protein G / genetics
  • S100 Calcium Binding Protein G / physiology*
  • Transfection*
  • Tumor Cells, Cultured

Substances

  • Calb1 protein, rat
  • Calbindin 1
  • Calbindins
  • Calcium Channels
  • Chelating Agents
  • S100 Calcium Binding Protein G
  • Calcium