Wu K K
Division of Hematology, The University of Texas-Houston Health Science Center, Medical School, 77030, USA.
Proc Assoc Am Physicians. 1998 May-Jun;110(3):163-70.
Nitric oxide (NO) and prostacyclin (PGI2) are potent molecules produced by endothelial cells that act synergistically to maintain normal vascular functions. Recent studies indicate that key enzymes that catalyze the synthesis of these two molecules are induced by chemical and physical factors. Because NO and PGI2 and their synthetic enzymes have short half-lives, transcriptional induction by injurious agents, such as lysophosphatidylcholine (lysoPC), represents an important defense mechanism. LysoPC is capable of inducing constitutive endothelial NO synthase (eNOS) and cyclooxygenase-2 (COX-2), an immediate early gene, with distinct kinetics and possibly distinct transcriptional mechanisms. The importance of injury-coupled eNOS and COX overexpression in vasoprotection is supported by powerful effects of virus-mediated transfer of COX and eNOS genes on defense against thrombosis and intimal hyperplasia in angioplasty-injured carotid arteries in animal models.
一氧化氮（NO）和前列环素（PGI2）是内皮细胞产生的强效分子，它们协同作用以维持正常的血管功能。最近的研究表明，催化这两种分子合成的关键酶是由化学和物理因素诱导产生的。由于NO、PGI2及其合成酶的半衰期较短，诸如溶血磷脂酰胆碱（lysoPC）等损伤因子的转录诱导代表了一种重要的防御机制。LysoPC能够诱导组成型内皮型一氧化氮合酶（eNOS）和环氧合酶-2（COX-2，一种即刻早期基因），其动力学不同，转录机制可能也不同。病毒介导的COX和eNOS基因转移对动物模型中血管成形术损伤的颈动脉的血栓形成和内膜增生具有强大的防御作用，这支持了损伤相关的eNOS和COX过表达在血管保护中的重要性。
