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Bcl‐x L overexpression restricts γ‐radiation‐induced apoptosis
Author(s) -
Wang ZiBing,
Zhang Ying,
Liu YuQing,
Guo Ying,
Xu Han,
Dong Bo,
Cui YuFang
Publication year - 2006
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2005.08.006
Subject(s) - apoptosis , ionizing radiation , bcl xl , transfection , immune system , reactive oxygen species , microbiology and biotechnology , mitochondrion , programmed cell death , biology , downregulation and upregulation , chemistry , gene , immunology , biochemistry , irradiation , physics , nuclear physics
Bcl‐x L 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‐x L 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‐x L proteins. Our results showed that overexpressed Bcl‐x L reduced time‐dependent increase of apoptosis induced by ionizing radiation. Reactive oxygen species (ROS) generation and Bax protein expression in the transfected AHH1‐Bcl‐x L 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.