text: Phospholipase C-γ1 is required for cell survival in oxidative stress by protein kinase C | Biochemical Journal
  Xiao-Chun BAI, Fan DENG, An-Ling LIU, Zhi-Peng ZOU, Yu WANG, Zhi-Yong KE, Qun-Sheng JI, Shen-Qiu LUO
  Biochemical Journal Apr 15, 2002, 363 (2) 395-401; DOI: 10.1042/bj3630395
  Department of Cell Biology and Medical Genetics, The First Military Medical University, Guangzhou 510515, People's Republic of China
  Department of Cell Biology and Medical Genetics, The First Military Medical University, Guangzhou 510515, People's Republic of ChinaDepartment of Biochemistry and Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232-0146, U.S.A.
  Phospholipase C-γ1 (PLC-γ1) activation has been reported to enhance cell survival during the cellular response to oxidative stress. We studied the role of protein kinase C (PKC) pathways in mediating PLC-γ1 survival signalling in oxidative stress by using mouse embryonic fibroblasts genetically deficient in PLC-γ1 (Plcg1−/−) and its wild type (Plcg1+/+). PLC-γ1 was activated by H2O2 treatment in a dose- and time-dependent manner. Activation of PKC was also markedly increased in both cell lines treated with H2O2 (1–5mM), but with low doses (50–200μM), PKC activation was considerably decreased in Plcg1−/− cells. After treatment with H2O2, PKC-dependent phosphorylation of Bcl-2 and cell viability of Plcg1−/− cells decreased dramatically and caspase-3-like activity increased significantly compared with that of the wild-type cells. Furthermore, pretreatment of Plcg1+/+ cells with PKC-specific inhibitor decreased levels of PKC-dependent Bcl-2 phosphorylation, enhanced caspase-3 activity and their sensitivity to H2O2. On the contrary, treatment of Plcg1−/− cells with PKC-specific activator increased the Bcl-2 phosphorylation, decreased caspase-3 activity and improved their survival. These results suggest that PLC-γ1 mediates survival signalling in oxidative-stress response by PKC-dependent phosphorylation of Bcl-2 and inhibition of caspase-3.
  Abbreviations used: DAG, diacylglycerol; ERK, extracellular signal-regulated kinase; MEF, mouse embryonic fibroblasts; PI-3K, phosphoinositide 3-kinase; PKC, protein kinase C; PLC-γ1, phospholipase C-γ1; Plcg1−/− and Plcg1+/+, MEF genetically deficient in PLC-γ1 and its wild type; PTK, protein tyrosine kinase.
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