TY - JOUR
T1 - Effects of radiation on Ca2+ signaling in salivary epithelial cell lines transfected with Bcl-2 and Bcl-XL
AU - Sun, Xiuhua
AU - Liu, Xiao Bing
AU - Martinez, J. Ricardo
AU - Dang, Howard
AU - Zhang, Guo H.
PY - 2001/4
Y1 - 2001/4
N2 - The effects of radiation on the Ca2+ signaling system in HSY cells transfected with the Bcl-2 or Bel-XL gene were studied. Bcl-2 overexpression did not alter carbachol (CCh)-elicited initial increase in cytosolic free Ca2+ concentrations ([Ca2+]i), but Bel-XL overexpression dramatically reduced this response. Exposure to 10 Gy γ-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 Bel-XL transfectants. The capacity of the IP3-sensitive Ca2+ store was significantly reduced by radiation in all cells except Bel-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 Bel-XL partially protects cells from radiation-induced inhibition of Ca2+ signaling.
AB - The effects of radiation on the Ca2+ signaling system in HSY cells transfected with the Bcl-2 or Bel-XL gene were studied. Bcl-2 overexpression did not alter carbachol (CCh)-elicited initial increase in cytosolic free Ca2+ concentrations ([Ca2+]i), but Bel-XL overexpression dramatically reduced this response. Exposure to 10 Gy γ-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 Bel-XL transfectants. The capacity of the IP3-sensitive Ca2+ store was significantly reduced by radiation in all cells except Bel-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 Bel-XL partially protects cells from radiation-induced inhibition of Ca2+ signaling.
KW - Bcl-2
KW - Bcl-XL
KW - Ca release and influx
KW - HSY cells
KW - IP formation
UR - http://www.scopus.com/inward/record.url?scp=0035318171&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035318171&partnerID=8YFLogxK
U2 - 10.1034/j.1600-0722.2001.00982.x
DO - 10.1034/j.1600-0722.2001.00982.x
M3 - Article
C2 - 11347653
AN - SCOPUS:0035318171
VL - 109
SP - 103
EP - 108
JO - European Journal of Oral Sciences
JF - European Journal of Oral Sciences
SN - 0909-8836
IS - 2
ER -