Xu Q, Liu Y, Gorospe M, Udelsman R, Holbrook N J
Section on Gene Expression and Aging, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA.
J Clin Invest. 1996 Jan 15;97(2):508-14. doi: 10.1172/JCI118442.
Mitogen-activated protein (MAP) kinases are rapidly activated in cells stimulated with various extracellular signals by dual phosphorylation of tyrosine and threonine residues. They are thought to play a pivotal role in transmitting transmembrane signals required for cell growth and differentiation. Herein we provide evidence that two distinct classes of MAP kinases, the extracellular signal-regulated kinases (ERK) and the c-Jun NH2-terminal kinases (JNK), are transiently activated in rat arteries (aorta, carotid and femoral arteries) in response to an acute elevation in blood pressure induced by either restraint or administration of hypertensive agents (i.e., phenylephrine and angiotensin II). Kinase activation is followed by an increase in c-fos and c-jun gene expression and enhanced activating protein 1 (AP-1) DNA-binding activity. Activation of ERK and JNK could contribute to smooth muscle cell hypertrophy/hyperplasia during arterial remodeling due to frequent and/or persistent elevations in blood pressure.
丝裂原活化蛋白（MAP）激酶在受到各种细胞外信号刺激的细胞中，通过酪氨酸和苏氨酸残基的双重磷酸化而迅速被激活。它们被认为在传递细胞生长和分化所需的跨膜信号中起关键作用。在此我们提供证据表明，两类不同的MAP激酶，即细胞外信号调节激酶（ERK）和c-Jun氨基末端激酶（JNK），在大鼠动脉（主动脉、颈动脉和股动脉）中因束缚或给予高血压药物（即去氧肾上腺素和血管紧张素II）诱导的血压急性升高而被短暂激活。激酶激活之后是c-fos和c-jun基因表达增加以及活化蛋白1（AP-1）DNA结合活性增强。由于血压频繁和/或持续升高，ERK和JNK的激活可能在动脉重塑过程中导致平滑肌细胞肥大/增生。
