Bishop-Bailey D, Hla T, Mitchell J A
Center for Vascular Biology, Department of Physiology, University of Connecticut Health Center, Farmington, CT 06030-3505, USA.
Int J Mol Med. 1999 Jan;3(1):41-8. doi: 10.3892/ijmm.3.1.41.
Two isoforms of cyclo-oxygenase (COX) have been identified; a constitutive isoform (COX-1), found in abundance in platelets and the vascular endothelium, considered important for the roles of prostanoids and a cytokine/mitogen inducible isoform (COX-2), which is thought responsible for the majority of the inflammatory prostanoid production. As a number of COX metabolites regulate vascular smooth muscle cell function and the interaction between the vessel and circulating components, we have discussed the possibility that COX-2 can be induced in, and regulate human arterial or venous smooth muscle cell function. It is now clear that COX-2 can be induced in freshly isolated vessels in culture, which can be further stimulated by addition of pro-inflammatory cytokines. Interestingly, smooth muscle cells derived from saphenous vein can release extremely high levels of prostanoids, and express greater levels of COX-2 protein than internal mammary artery cells. This difference can be accounted for by an arterial cell-specific negative feedback mechanism. In addition to inducing COX-2, certain cytokines regulate smooth muscle function, by regulating cell proliferation, adhesion, and mediator release. The effects of COX-2 activity on these smooth muscle cell responses will be further discussed.
已鉴定出环氧化酶（COX）的两种同工型；一种组成型同工型（COX-1），在血小板和血管内皮中大量存在，被认为对前列腺素和细胞因子/丝裂原的作用很重要，以及一种细胞因子/丝裂原诱导型同工型（COX-2），它被认为是大多数炎性前列腺素产生的原因。由于许多COX代谢产物调节血管平滑肌细胞功能以及血管与循环成分之间的相互作用，我们讨论了COX-2在人动脉或静脉平滑肌细胞中被诱导并调节其功能的可能性。现在很清楚，COX-2可在培养的新鲜分离血管中被诱导，添加促炎细胞因子可进一步刺激这种诱导。有趣的是，来自大隐静脉的平滑肌细胞可释放极高水平的前列腺素，并且比乳内动脉细胞表达更高水平的COX-2蛋白。这种差异可由动脉细胞特异性负反馈机制来解释。除了诱导COX-2外，某些细胞因子还通过调节细胞增殖、黏附及介质释放来调节平滑肌功能。将进一步讨论COX-2活性对这些平滑肌细胞反应的影响。
