Involvement of phospholipase D in oxidative stress‐induced necrosis of vascular smooth muscle cells

FEBS Letters

Shin, Eun-Young²  Hyun, Min-Soo²  Kim, Hun-Sik³  Kim, Eung-Gook²  Shin, Kyung-Sun²  Min, Do Sik¹  Ha, Kwon-Soo⁴  Ahn, Hee-Yul³  Shin, Ji-Cheol¹ 

[1] Department of Physiology, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Socho-gu, Seoul 137-701, South Korea;Department of Biochemistry, College of Medicine and Research Institute for Genetic Engineering, Chungbuk National University, San 48, Gaesin-dong, Heungduk-ku, Cheongju 361-763, South Korea;Department of Pharmacology, College of Medicine, Chungbuk National University, Cheongju 361-763, South Korea;Biomolecule Research Group, Korea Basic Science Institute, Taejon 305-333, South Korea

关键词: Phospholipase D;    Pervanadate;    Necrosis;    Vascular smooth muscle cell;   

DOI  :  10.1016/S0014-5793(01)03059-9

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Phospholipase D (PLD) has been associated with necrosis. However, it is not clear whether PLD plays a causative role in this cellular process. We investigated the role of PLD in oxidative stress-induced necrosis of vascular smooth muscle cells (VSMCs). Pervanadate (hydrogen peroxide plus orthovanadate) but not hydrogen peroxide alone activated PLD in a dose- and time-dependent manner. Exposure of VSMCs to pervanadate resulted in necrosis. Pretreatment with butan-1-ol, a PLD inhibitor, attenuated both pervanadate-induced necrosis and increase of intracellular Ca²⁺. Removal of extracellular Ca²⁺ inhibited pervanadate-induced necrosis by 50%. These results suggest that PLD activation mediates pervanadate-induced necrosis of VSMCs, which is at least partly due to Ca²⁺ toxicity.

【 授权许可】

Unknown