Bcl-xL overexpression restricts gamma-radiation-induced apoptosis |
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Authors: | Wang Zi-Bing Zhang Ying Liu Yu-Qing Guo Ying Xu Han Dong Bo Cui Yu-Fang |
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Affiliation: | Department of Immunology, Beijing Institute of Radiation Medicine, 27 Taiping Road, 100850 Beijing, China. |
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Abstract: | 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. |
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Keywords: | Radiation Apoptosis Bcl‐xL Bax ROS MMP |
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