Bcl-xL overexpression restricts gamma-radiation-induced apoptosis.

Cell Biol Int

Department of Immunology, Beijing Institute of Radiation Medicine, 27 Taiping Road, 100850 Beijing, China.

Published: January 2006

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.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.cellbi.2005.08.006DOI Listing

Publication Analysis

Top Keywords

ionizing radiation
8
immune injury
8
ahh-1 cells
8
bcl-xl
5
bcl-xl overexpression
4
overexpression restricts
4
restricts gamma-radiation-induced
4
apoptosis
4
gamma-radiation-induced apoptosis
4
apoptosis bcl-xl
4

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!