Effects of radiation on Ca2+ signaling in salivary epithelial cell lines transfected with Bcl-2 and Bcl-XL.
Effects of radiation on Ca2+ signaling in salivary epithelial cell lines transfected with Bcl-2 and Bcl-XL.
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DOI：
10.1034/j.1600-0722.2001.00982.x
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发表时间：
2001-04
影响因子：
1.9
通讯作者：
X. Sun;X. Liu;J. R. Martinez;H. Dang;G. H. Zhang
中科院分区：
文献类型：
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作者：
X. Sun;X. Liu;J. R. Martinez;H. Dang;G. H. Zhang
研究了辐射对转染Bcl-2或Bcl-XL基因的HSY细胞Ca2+信号系统的影响。Bcl-2过表达不会改变碳水化合物（CCh）引起的胞质游离Ca2+浓度（[Ca2+]i）的初始升高，但Bcl-XL过表达会显著降低这种反应。暴露于10 Gy γ射线中不改变基底[Ca2+]i。相比之下，cch刺激的初始[Ca2+]i增加在照射后0.5和4 h在所有细胞类型中都有所减少，在野生型和对照转染的细胞中在24 h仍然下降，但在Bcl-2-和bcl - xl -转染的细胞中恢复。野生型和对照转染的细胞在辐照后4小时对CCh的反应中肌醇1,4,5-三磷酸（IP3）的形成减少，但在Bcl-2和Bcl-XL转染的细胞中没有。除Bcl-XL外，所有细胞的ip3敏感Ca2+储存能力都被辐射显著降低。在野生型和对照转染的细胞中，CCh刺激后的Ca2+内流被暴露于辐射抑制，但在Bcl-2-和bcl - xl -转染细胞中没有。然而，辐射增强了所有细胞类型中由thapsigargin激活的Ca2+内流。这些结果表明：1)辐射减少了响应于CCh的IP3形成和Ca2+释放，但增强了储存操作的Ca2+内流；2) Bcl-2或Bcl-XL的过表达部分保护细胞免受辐射诱导的Ca2+信号抑制。
The effects of radiation on the Ca2+ signaling system in HSY cells transfected with the Bcl-2 or Bcl-XL gene were studied. Bcl-2 overexpression did not alter carbachol (CCh)-elicited initial increase in cytosolic free Ca2+ concentrations ([Ca2+]i), but Bcl-XL overexpression dramatically reduced this response. Exposure to 10 Gy gamma-ray did not alter basal [Ca2+]i. By contrast, the CCh-stimulated initial [Ca2+]i increase was reduced at 0.5 and 4 h post-irradiation in all cell types and remained decreased at 24 h in wild-type and control-transfected cells, but recovered in Bcl-2- and Bcl-XL-transfectants. The formation of inositol 1,4,5-trisphosphate (IP3) in response to CCh at 4-h post-irradiation was decreased in wild-type and control-transfected cells, but not in Bcl-2 and Bcl-XL transfectants. The capacity of the IP3-sensitive Ca2+ store was significantly reduced by radiation in all cells except Bcl-XL transfectants. Ca2+ influx after stimulation with CCh was suppressed by exposure to radiation in wild-type and control-transfected cells, but not in Bcl-2- and Bcl-XL-transfectants. However, radiation enhanced Ca2+ influx activated by thapsigargin in all cell types. These results suggest that 1) radiation diminishes IP3 formation and Ca2+ release in response to CCh, but potentiates the store-operated Ca2+ influx; and 2) overexpression of Bcl-2 or Bcl-XL partially protects cells from radiation-induced inhibition of Ca2+ signaling.