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Primary study on the lesions and specific proteins in BEAS-2B cells induced with the 2009 A (H1N1) influenza virus
Authors:Shisong Fang  Kaining Zhang  Ting Wang  Xin Wang  Xing Lu  Bo Peng  Weihua Wu  Ran Zhang  Shiju Chen  Renli Zhang  Hong Xue  Muhua Yu  Jinquan Cheng
Institution:1. Shenzhen Centre for Disease Control and Prevention, No. 8, LongYuan Rd., NanShan District, Shenzhen City, Guangdong Province, People’s Republic of China
3. Shandong Provincial Qianfoshan Hospital, Jinan, People’s Republic of China
2. Shenzhen Nanshan Centre for Disease Control and Prevention, Shenzhen, People’s Republic of China
4. Hong Kong University of Science and Technology, Kowloon, Hong Kong
5. Division of Microbiology Test, Shenzhen Nanshan Centre for Disease Control and Prevention, No. 95, Nanshang Rd., Nanshan District, Shenzhen City, Guangdong Province, People’s Republic of China
Abstract:In order to investigate the lesions and proteins with differential expression in cells infected with the 2009 A (H1N1) virus and to determine the specific proteins involved in cell damage, the present study has been performed. BEAS-2B cells were infected with the 2009 A (H1N1) influenza virus or the seasonal H1N1 influenza virus for 12, 24, 48, and 72 h, and cell cycle and apoptosis were analyzed with flow cytometry. Total cellular proteins were extracted and underwent two-dimensional gel electrophoresis. The differentially expressed proteins underwent mass spectrometry for identification. The results showed that after 12 h, cells infected with the virus strain sourced from severe cases had the highest apoptosis rate (P?P?P?Galectin-1 was specifically observed in BEAS-2B infected with 2009 A (H1N1) influenza viruses, and cofilin-1 was specifically observed in BEAS-2B cells in the late stage of 2009 A (H1N1) influenza virus infection. In conclusion, differential effects of the 2009 A (H1N1) influenza virus and seasonal H1N1 influenza virus were identified on the cell cycle and apoptosis, and galectin-1 may play a role in cell apoptosis induced by 2009 A (H1N1) influenza virus.
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