Activation of protein kinase C is required for protection of cells against apoptosis induced by singlet oxygen

FEBS Letters

Kochevar, Irene E¹  Lynch, Mary C¹  Zhuang, Shougang¹ 

[1] Wellman Laboratories of Photomedicine, Massachusetts General Hospital, Harvard Medical School, WEL-224, 55 Fruit St., Boston MA 02114, USA

关键词: Protein kinase C;    Apoptosis;    Singlet oxygen;    Extracellular signal-regulated kinase;    Rose bengal;    HL-60 cell;    PKC;    protein kinase C;    ERK;    extracellular signal-regulated kinase;    MEK;    ERK kinase;    JNK;    c-jun NH2-terminal kinase;    TPA;    12-O-tetradecanoyl phorbol 13-acetate;    DMEM;    Dulbecco's modified Eagle's medium;    RB;    rose bengal;   

DOI  :  10.1016/S0014-5793(98)01222-8

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

We evaluated the role of protein kinase C (PKC) in the regulation of apoptosis triggered by singlet oxygen. Activation of PKC by short-term 12-O-tetradecanoyl phorbol 13-acetate (TPA) treatment inhibited apoptosis, whereas inhibition of PKC with several inhibitors potentiated this process. The antiapoptotic effect of TPA was accompanied by phosphorylation of extracelluar signal-regulated kinase 1/2 (ERK1/2). Pretreatment of cells with MEK inhibitor, PD98059, inhibited TPA-induced phosphorylation of ERK1/2 and the cytoprotective ability of TPA. These results suggest that activation of PKC in HL-60 cells confers protection against apoptosis induced by singlet oxygen and that ERK1/2 mediates antiapoptotic signaling of PKC.

【 授权许可】

Unknown