Effects of radiation on Ca 2+ signaling in salivary epithelial cell lines transfected with Bcl‐2 and Bcl‐XL

The effects of radiation on the Ca 2+ 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 Ca 2+ concentrations ([Ca 2+ ] i ), but Bcl‐XL overexpression dramatically reduce...

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Published inEuropean journal of oral sciences Vol. 109; no. 2; pp. 103 - 108
Main Authors Sun, Xiuhua, Liu, Xiao‐bing, Martinez, J. Ricardo, Dang, Howard, Zhang, Guo H.
Format Journal Article
LanguageEnglish
Published 01.04.2001
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Summary:The effects of radiation on the Ca 2+ 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 Ca 2+ concentrations ([Ca 2+ ] i ), but Bcl‐XL overexpression dramatically reduced this response. Exposure to 10 Gy γ‐ray did not alter basal [Ca 2+ ] i . By contrast, the CCh‐stimulated initial [Ca 2+ ] 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 (IP 3 ) 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 IP 3 ‐sensitive Ca 2+ store was significantly reduced by radiation in all cells except Bcl‐XL transfectants. Ca 2+ 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 Ca 2+ influx activated by thapsigargin in all cell types. These results suggest that 1) radiation diminishes IP 3 formation and Ca 2+ release in response to CCh, but potentiates the store‐operated Ca 2+ influx; and 2) overexpression of Bcl‐2 or Bcl‐XL partially protects cells from radiation‐induced inhibition of Ca 2+ signaling.
ISSN:0909-8836
1600-0722
DOI:10.1034/j.1600-0722.2001.00982.x