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肌醇1,4,5-三磷酸和花生四烯酸诱导的T和B淋巴细胞中的钙动员。

Inositol 1,4,5-trisphosphate- and arachidonic acid-induced calcium mobilization in T and B lymphocytes.

作者信息

Corado J, Le Deist F, Griscelli C, Fischer A

机构信息

INSERM U 132, Hôpital Necker-Enfants Malades, Paris, France.

出版信息

Cell Immunol. 1990 Apr 1;126(2):245-54. doi: 10.1016/0008-8749(90)90318-l.

DOI:10.1016/0008-8749(90)90318-l
PMID:2107029
Abstract

Inositol triphosphate (IP3) formation and increase in intracytoplasmic calcium are mediators of signal transduction in lymphocytes. It has been proposed that IP3 induces Ca2+ release from intracellular stores. It is in order to study the relationship between these two events that we have analyzed the effect of IP3 addition on Ca2+ mobilization in permeabilized resting T and B lymphocytes, EBV-B lymphocytes, and HTLV1-T lymphocytes. IP3 induces a rapid and significant release of Ca2+ from the endoplasmic reticulum in a dose-dependent manner. Ca2+ release is more sensitive to IP3 addition in cycling cells (EBV-B lymphocytes and HTLV1-T lymphocytes) than in resting T and B lymphocytes. Arachidonic acid (AA) induces Ca2+ release from the endoplasmic reticulum (ER) in a manner similar to that of IP3. Neither component has an effect on Ca2+ accumulated in mitochondria, and they have no additive effects suggesting that they act on a similar Ca2+ pool. These results directly demonstrate that in T and B human lymphocytes IP3 mobilizes Ca2+ from ER as in other cellular systems and that other potential second messengers, namely AA, could play a significant role in the internal mobilization of calcium during T and B lymphocyte activation.

摘要

肌醇三磷酸(IP3)的形成以及胞浆内钙离子的增加是淋巴细胞信号转导的介质。有人提出IP3可诱导细胞内储存的Ca2+释放。正是为了研究这两个事件之间的关系,我们分析了添加IP3对通透的静止T和B淋巴细胞、EBV - B淋巴细胞以及HTLV1 - T淋巴细胞中Ca2+动员的影响。IP3以剂量依赖的方式诱导内质网快速且显著地释放Ca2+。与静止的T和B淋巴细胞相比,循环细胞(EBV - B淋巴细胞和HTLV1 - T淋巴细胞)中Ca2+释放对添加IP3更为敏感。花生四烯酸(AA)以类似于IP3的方式诱导内质网(ER)释放Ca2+。两者对线粒体中积累的Ca2+均无影响,且它们没有相加效应,这表明它们作用于相似的Ca2+池。这些结果直接证明,在人类T和B淋巴细胞中,IP3如同在其他细胞系统中一样从内质网动员Ca2+,并且其他潜在的第二信使,即AA,可能在T和B淋巴细胞激活过程中钙的内部动员中发挥重要作用。

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