close functional coupling between ca2+ release-activated ca2+ channels and reactive oxygen species production in murine macrophages关闭功能之间的耦合ca2 + release-activated ca2 +渠道和小鼠巨噬细胞的活性氧产量.pdfVIP

Hindawi Publishing Corporation Mediators of Inflammation Volume 2006, Article ID 36192, Pages 1–8 DOI 10.1155/MI/2006/36192 Research Article Close Functional Coupling Between Ca2+ Release-Activated Ca2+ Channels and Reactive Oxygen Species Production in Murine Macrophages Sheng-Wei Jin,1, 2 Li Zhang,3 Qin-Quan Lian,2 Shang-Long Yao,1 Ping Wu,3 Xiao-Yan Zhou,3 Wei Xiong,3 and Du-Yun Ye3 1 Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China 2 Department of Anesthesiology, Second Affi liated Hospital, Wenzhou Medical College, Wenzhou 325027, China 3 Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China Received 14 June 2006; Revised 9 September 2006; Accepted 10 September 2006 Aim . To investigate the role of Ca2+ release-activated Ca2+ (CRAC) channels in the ROS production in macrophages. Methods. The intracellular [Ca2+ ] was analyzed by confocal laser microscopy. The production of ROS was assayed by flow cytometry. Results. i Both LPS and thapsigargin induced an increase in intracellular [Ca2+ ] , either in the presence or absence of extracellular Ca2+ in i murine macrophages. The Ca2+ signal was sustained in the presence of external Ca2+ and only initiated a mild and transient rise in the absence of external Ca2+ . CRAC channel inhibitor 2-APB completely suppressed the Ca2+ entry signal evoked by thapsigargin, and suppressed approximately 93% of the Ca2+ entry signal evoked by LPS. The increase in intracellular [Ca2+ ] was associated