Acute hypertension activates mitogen-activated protein kinases arterial wall
Acute hypertension activates mitogen-activated protein kinases arterial wall
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DOI：
10.1172/jci118442
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发表时间：
1996-01-15
影响因子：
15.9
通讯作者：
Holbrook, NJ
中科院分区：
文献类型：
--
作者：
Xu, QB;Liu, YS;Holbrook, NJ
丝裂原活化蛋白(MAP)激酶在各种细胞外信号的刺激下，通过酪氨酸和苏氨酸残基的双重磷酸化而迅速激活。它们被认为在传递细胞生长和分化所需的跨膜信号方面起着关键作用，在这里，我们提供了两种不同类型的MAP激酶，细胞外信号调节激酶(ERK)和c-Jun NH2末端激酶(JNK)在大鼠动脉(主动脉、颈动脉和股动脉)中被瞬时激活，以响应由束缚或给药高血压药物(即苯肾上腺素和血管紧张素II)引起的血压急剧升高。激酶激活后，c-fos和c-jun基因表达增加，激活蛋白1(AP-1)DNA结合活性增强。在动脉重塑过程中，由于血压的频繁和/或持续升高，ERK和JNK的激活可能参与了血管平滑肌细胞的肥大/增殖。
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.