Pearce M J, McIntyre T M, Prescott S M, Zimmerman G A, Whatley R E
Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah School of Medicine, Salt Lake City 84112, USA.
Biochem Biophys Res Commun. 1996 Jan 17;218(2):500-4. doi: 10.1006/bbrc.1996.0089.
Intracellular signalling events that govern endothelial responses to shear are incompletely defined. In this study confluent human endothelial cells were subjected to shear. At shear levels of 1.04, 2.92, 5.31 and 8.3 dynes/cm2, which are in the range of those that occur in vessels in venous and arterial circulations, the activity of cPLA2 was increased above control levels. To examine pathways by which cPLA2 may be activated in response to shear, we assayed the p42 isoform of MAP kinase (ERK-2) and found increased activity in cells exposed to shear. Our findings demonstrate for the first time that cPLA2 and MAP kinase p42 are activated by shear in human endothelial cells, and add to evidence from other systems that indicates that the two enzymes have related signalling functions.
调控内皮细胞对剪切力反应的细胞内信号转导事件尚未完全明确。在本研究中,将汇合的人内皮细胞置于剪切力作用下。在1.04、2.92、5.31和8.3达因/平方厘米的剪切力水平下,这些水平处于静脉和动脉循环中血管所出现的范围内,胞质型磷脂酶A2(cPLA2)的活性高于对照水平。为了研究cPLA2可能响应剪切力而被激活的途径,我们检测了丝裂原活化蛋白激酶(ERK-2)的p42亚型,发现在暴露于剪切力的细胞中其活性增加。我们的研究结果首次证明,cPLA2和丝裂原活化蛋白激酶p42在人内皮细胞中被剪切力激活,并补充了来自其他系统的证据,表明这两种酶具有相关的信号传导功能。