Bcl-xL overexpression restricts gamma-radiation-induced apoptosis.
Bcl-xL belongs to a family of proteins which inhibit apoptosis in a number of stimuli including ionizing radiation. To better understand the effects and mechanisms of Bcl-xL on the apoptosis of lymphocytes and provide experimental basis to treat immune injury induced by radiation, we used normal human lymphoblastoid AHH-1 cells that were engineered to overexpress Bcl-xL proteins. Our results showed that overexpressed Bcl-xL reduced time-dependent increase of apoptosis induced by ionizing radiation. Reactive oxygen species (ROS) generation and Bax protein expression in the transfected AHH1-Bcl-xL cells were also lower compared to parental AHH-1 cells. Unexpectedly, the fluorescence intensity of Rhodomine 123 (Rh 123) for measuring mitochondrial membrane potential (MMP) did not change at all detected time points. These results possess a vital significance for insights into a new strategy for gene therapy of radiation-induced immune injury.
Wang
Zi-Bing
ZB
Department of Immunology, Beijing Institute of Radiation Medicine, 27 Taiping Road, 100850 Beijing, China.
Zhang
Ying
Y
Liu
Yu-Qing
YQ
Guo
Ying
Y
Xu
Han
H
Dong
Bo
B
Cui
Yu-Fang
YF
D017209:Apoptosis / Q000528:radiation effects*; D016923:Cell Death / Q000528:radiation effects; D002460:Cell Line; D004307:Dose-Response Relationship, Radiation; D005720:Gamma Rays; D006801:Humans; D008214:Lymphocytes / Q000502:physiology* / Q000528:radiation effects; D008564:Membrane Potentials; D051336:Mitochondrial Membranes / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D014162:Transfection; D051028:bcl-2-Associated X Protein / Q000378:metabolism; D051020:bcl-X Protein / Q000378:metabolism*
D017382:Reactive Oxygen Species; D051028:bcl-2-Associated X Protein; D051020:bcl-X Protein