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The cytosolic free calcium in anti‐μ‐stimulated human B cells is derived partly from extracellular medium and partly from intracellular stores
Author(s) -
Dugas Bernard,
Calenda Alphonse,
Delfraissy JeanFrançois,
Vazquez Aimé,
Bach JeanFrançois,
Galanaud Pierre
Publication year - 1987
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830170916
Subject(s) - extracellular , intracellular , inositol , egta , cytosol , endoplasmic reticulum , biology , calcium , stimulation , inositol phosphate , fura 2 , microbiology and biotechnology , calcium in biology , biochemistry , biophysics , inositol trisphosphate , plasma membrane ca2+ atpase , endocrinology , medicine , receptor , atpase , enzyme
Abstract The inositol phospholipid metabolism and the increase in cytosolic free Ca 2+ concentration ([Ca 2+ ] i ) into the cell are recognized as two important events in the anti‐μ‐induced B cell activation. The anti‐μ stimulation caused the [ 3 H]inositol incorporation and also a rapid increase in [Ca 2+ ] i from 85 nM to 285 nM. This signal returned to baseline a few minutes after stimulation. By using the fluorescent indicator quin‐2 we demonstrated that this [Ca 2+ ] i uptake was derived part from extracellular medium and part from intracellular stores. Both EGTA (a calcium chelator) and TMB.8 (a drug which interferes with Ca 2+ sequestration by smooth endoplasmic retiulum) partially suppressed the intracellular Ca 2+ uptake and were fully inhibitory when added together. The role of Ca 2+ from intracellular stores may also be evidenced in calcium‐free experiments, or in permeabilized experiments using exogenous inositol 1,4,5‐trisphosphate (IP 3 , the putative mobilizer of intracellular Ca 2+ ). Preventing the increase in [Ca 2+ ] i also prevents the apparition of early activation markers. These results are consistent with the hypothesis that the Ca 2+ increase in B cells stimulated by anti‐μ is caused by the generation of IP 3 during the phosphatidyl‐inositol metabolism and also by the entry of extracellular Ca 2+ through the plasma membrane.