Slow and persistent increase of [Ca2+]c in response to ligation of surface IgM in WEHI‐231 cells

FEBS Letters

Uhm, Dae-Yong¹  Kim, Tae Jin²  Yoon, Sang Soon²  Nam, Joo Hyun¹  Kim, Sung Joon¹ 

[1] Department of Physiology, Sungkyunkwan University School of Medicine, Changan-Gu, Cheoncheon-Dong, Suwon 440-746, Republic of Korea;Department of Pathology, Sungkyunkwan University School of Medicine, Suwon 440-746, Republic of Korea

关键词: B cell;    WEHI-231;    B cell antigen receptor;    Apoptosis;    Cytosolic Ca2+ concentration;    2-APB;    2-aminoethoxydiphenyl borate;    BCR;    B cell antigen receptor;    [Ca2+]c;    cytosolic Ca2+ concentration;    SOCE;    store-operated Ca2+ entry;    IP3;    inositol 1;    4;    5-trisphosphate;   

DOI  :  10.1016/S0014-5793(02)03884-X

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

WEHI-231 and Bal 17 B cell lines are representative models for immature and mature B cells, respectively. Their regulation of cytosolic Ca²⁺ concentration ([Ca²⁺]_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 [Ca²⁺]_c in WEHI-231 cells while not in Bal 17 cells. The thapsigargin-induced store-operated Ca²⁺ 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 [Ca²⁺]_c by BCR ligation was also enhanced by 2-APB in WEHI-231 cells while blocked in Bal 17 cells. The Mn²⁺ quenching study showed that the thapsigargin-, or the BCR ligation-induced Ca²⁺ influx pathway of WEHI-231 was hardly permeable to Mn²⁺. The intractable increase of [Ca²⁺]_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.

【 授权许可】

Unknown