ucp2 inhibits ros-mediated apoptosis in a549 under hypoxic conditions在缺氧条件下ucp2抑制ros-mediated在a549细胞凋亡.pdfVIP

UCP2 Inhibits ROS-Mediated Apoptosis in A549 under Hypoxic Conditions 1,2. 3. 1 1 1 4 1 Sanming Deng , Ye Yang , Yong Han , Xiaofei Li , Xiaoping Wang , Xueyong Li , Zhipei Zhang , Yunjie Wang1* 1 Department of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi’an, Shaanxi Province, China, 2 Department of Thoracic Surgery, The Hospital of Medical College of Chinese People’s Armed Police Force, Tianjin, China, 3 Department of Thoracic Surgery, Shaanxi Province People’s Hospital, Xi’an, Shaanxi Province, China, 4 Department of Plastics and Burns, Tangdu Hospital, The Fourth Military Medical University, Xi’an, Shaanxi Province, China Abstract The Crosstalk between a tumor and its hypoxic microenvironment has become increasingly important. However, the exact role of UCP2 function in cancer cells under hypoxia remains unknown. In this study, UCP2 showed anti-apoptotic properties in A549 cells under hypoxic conditions. Over-expression of UCP2 in A549 cells inhibited reactive oxygen species (ROS) accumulation (P,0.001) and apoptosis (P,0.001) compared to the controls when the cells were exposed to hypoxia. Moreover, over-expression of UCP2 inhibited the release of cytochrome C and reduced the activation of caspase-9. Conversely, suppression of UCP2 resulted in the ROS generation (P = 0.006), the induction of apoptosis (P,0.001), and the release of cytochrome C from mitochondria to the cytosolic fraction, thus activating caspase-9. These data suggest that over-expression of UCP2 has anti-apoptotic properties by inhibiting ROS-mediated apoptosis in A549 cells under hypoxic conditions. Citation: Deng S, Yang Y, Han Y, Li X, Wang X, et al. (2012) UCP2