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Slow and persistent increase of [Ca 2+ ] c in response to ligation of surface IgM in WEHI‐231 cells
Author(s) -
Nam Joo Hyun,
Yoon Sang Soon,
Kim Tae Jin,
Uhm Dae-Yong,
Kim Sung Joon
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(02)03884-x
Subject(s) - thapsigargin , chemistry , breakpoint cluster region , microbiology and biotechnology , jurkat cells , cytosol , apoptosis , cell culture , ligation , receptor , medicine , t cell , immunology , biology , biochemistry , endoplasmic reticulum , immune system , genetics , enzyme
WEHI‐231 and Bal 17 B cell lines are representative models for immature and mature B cells, respectively. Their regulation of cytosolic Ca 2+ concentration ([Ca 2+ ] c ) was compared using fura‐2 fluorescence ratiometry. The ligation of B cell antigen receptor (BCR) by anti‐IgM antibody induced a slow but large increase of [Ca 2+ ] c in WEHI‐231 cells while not in Bal 17 cells. The thapsigargin‐induced store‐operated Ca 2+ entry (SOCE) of Bal 17 cells reached a steady state which was blocked by 2‐aminoethoxydiphenyl borate (2‐APB). On the contrary, the thapsigargin‐induced SOCE of WEHI‐231 cells increased continuously, which was accelerated by 2‐APB. The increase of [Ca 2+ ] c by BCR ligation was also enhanced by 2‐APB in WEHI‐231 cells while blocked in Bal 17 cells. The Mn 2+ quenching study showed that the thapsigargin‐, or the BCR ligation‐induced Ca 2+ influx pathway of WEHI‐231 was hardly permeable to Mn 2+ . The intractable increase of [Ca 2+ ] c may explain the mechanism of BCR‐driven apoptosis of WEHI‐231 cells, a well‐known model of clonal deletion of autoreactive immature B cells.