Differentiation of BC3H1 smooth muscle cells changes the bivalent cation selectivity of the capacitative Ca2+ entry pathway.
Differentiation of BC3H1 smooth muscle cells changes the bivalent cation selectivity of the capacitative Ca2+ entry pathway.
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BC3H1 平滑肌细胞的分化改变了电容性 Ca2+ 进入途径的二价阳离子选择性。
DOI：
10.1042/bj3160759
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
C. Taylor
中科院分区：
文献类型：
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作者：
L. Broad;D. Powis;C. Taylor
BC 3 H1细胞的分化导致平滑肌的各种蛋白质特征的表达和细胞内Ca 2+商店的行为的变化。用毒胡萝卜素（2 μ M）处理分化和未分化的细胞，清空其细胞内Ca 2+储存，并在细胞外Ca 2+存在下引起细胞溶质[Ca 2 +]增加，其去除后迅速逆转。这些容量性Ca 2+进入信号的幅度在分化细胞中为101 +/- 8 nM（n = 42），在未分化细胞中为188 +/- 16 nM（n = 35）。通过记录胞质fura 2荧光猝灭测量的毒胡萝卜素处理的细胞中的Mn 2+进入，在分化和未分化细胞中分别为对照率的374 +/- 26%（n = 34）和154 +/- 7%（n = 41）。空储存导致Ba 2+进入在分化细胞中增加到其基础速率的282 +/-20%（n = 8），在未分化细胞中增加到187 +/-20%（n = 8）。在快速去除细胞外Ca 2+（其中容量性Ca 2+进入已被激活）后测量的Ca 2+排出率在分化（t1/2 = 23 +/- 2 s，n = 7）和未分化（23 +/- 1 s，n = 6）细胞中相似。因此，电容性Ca 2+和Mn 2+信号之间的不同关系不是分化细胞中更活跃的Ca 2+挤出机制的结果，也不是两种细胞类型中不同的fura 2负载的结果。我们得出结论，在BC 3 H1细胞的分化过程中，电容途径的阳离子选择性发生变化，变得对Mn 2+和Ba 2+相对更具有渗透性。这种变化可能是由于不同的容量途径的表达或单个途径的渗透性质的改变。
Differentiation of BC3H1 cells leads to expression of a variety of proteins characteristic of smooth muscle and to changes in the behaviour of intracellular Ca2+ stores. Treatment of both differentiated and undifferentiated cells with thapsigargin (2 microM) emptied their intracellular Ca2+ stores, and in the presence of extracellular Ca2+ caused an increase in cytosolic [Ca2+] that rapidly reversed after its removal. The amplitudes of these capacitative Ca2+ entry signals were 101 +/- 8 nM (n = 42) in differentiated cells and 188 +/- 16 nM (n = 35) in undifferentiated cells. Mn2+ entry in thapsigargin-treated cells, measured by recording the quenching of cytosolic fura 2 fluorescence, was 374 +/- 26% (n = 34) and 154 +/- 7% (n = 41) of control rates in differentiated and undifferentiated cells, respectively. Empty stores caused Ba2+ entry to increase to 282 +/- 20% (n = 8) of its basal rate in differentiated cells and to 187 +/- 20% (n = 8) in undifferentiated cells. Rates of Ca2+ extrusion, measured after rapid removal of extracellular Ca2+ from cells in which capacitative Ca2+ entry had been activated, were similar in differentiated (t1/2 = 23 +/- 2 s, n = 7) and undifferentiated (23 +/- 1 s, n = 6) cells. The different relationships between capacitative Ca2+ and Mn2+ signals are not, therefore, a consequence of more active Ca2+ extrusion mechanisms in differentiated cells, nor are they a consequence of different fura 2 loadings in the two cell types. We conclude that during differentiation of BC3Hl cells, the cation selectivity of the capacitative pathway changes, becoming relatively more permeable to Mn2+ and Ba2+. The change may result either from expression of a different capacitative pathway or from modification of the permeation properties of a single pathway.