Regulation of endoplasmic reticulum-Ca-ATPase by glycolysis in eukaryotic cells

Miner Electrolyte Metab. 1996;22(5-6):318-35.

Abstract

This paper reviews work by our and other laboratories that explores the coupling between glycolysis and endoplasmic reticulum (ER)-Ca-ATPases in regulating Ca2+ homeostasis in several cell types. Changes in intracellular Ca2+ [(Ca2+]in) link interaction between hormones and cell surface receptors with the initiation of specific cellular functions. Thus, changes in [Ca2+]in mediate signal transduction mechanisms that modulate many physiological functions including cell growth, muscle cell contractility, and exocytosis in secretory cells. In most eukaryotic cells, total cellular Ca2+ is in the millimolar range, yet only a fraction (i.e., nanomolar) is free in the cytosol. Cells use both active and 'passive' mechanisms to maintain [Ca2+]in within a narrow range. Active mechanisms include plasma membrane and endoplasmic/sarcoplasmic reticulum (ER/SR)-Ca-ATPases, Ca2+ channels (inositol trisphosphate- and voltage-sensitive), and Na+/Ca2+ exchangers. 'Passive' mechanisms include Ca(2+)-binding proteins (e.g., calsequestrin, calmodulin, calreticulin). The relative contribution of active and 'passive' mechanisms to [Ca2+]in homeostasis in a given cell is not known. Ca2+ might move among several intracellular compartments, including the ER/SR, mitochondria, nucleus, Golgi apparatus, endosomes and lysosomes. The ubiquitous distribution of ER-Ca-ATPases in these intracellular organelles suggests a major role of this pump in Ca2+ homeostasis, but the importance of intracellular compartments to [Ca2+]in homeostasis is not well understood. Glucose has been suggested to have a role in regulating some of these ion transport processes. Thus, the increased cell metabolism that follows glucose stimulation is associated with altered [Ca2+]in homeostasis. The precise mechanisms by which glucose or its metabolites modulate [Ca2+]in homeostasis are unknown but might involve regulation of ER-Ca-ATPases.

Publication types

  • Review

MeSH terms

  • Calcium / metabolism
  • Calcium-Transporting ATPases / antagonists & inhibitors
  • Calcium-Transporting ATPases / metabolism*
  • Cells, Cultured
  • Endoplasmic Reticulum / enzymology*
  • Eukaryotic Cells / enzymology*
  • Glucose / physiology
  • Glycolysis*
  • Homeostasis
  • Hydrogen-Ion Concentration
  • Indoles / pharmacology
  • Insulin / metabolism
  • Insulin Secretion
  • Intracellular Membranes / metabolism
  • Muscle Contraction
  • Muscle, Smooth, Vascular / physiology
  • Thapsigargin / pharmacology

Substances

  • Indoles
  • Insulin
  • Thapsigargin
  • Calcium-Transporting ATPases
  • Glucose
  • Calcium
  • cyclopiazonic acid