Ushio-Fukai Masuko, Alexander R Wayne
Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
Mol Cell Biochem. 2004 Sep;264(1-2):85-97. doi: 10.1023/b:mcbi.0000044378.09409.b5.
Angiogenesis, a process of new blood vessel growth, contributes to various pathophysiologies such as cancer, diabetic retinopathy and atherosclerosis. Accumulating evidence suggests that cardiovascular diseases are associated with increased oxidative stress in blood vessels. Reactive oxygen species (ROS) such as superoxide and H2O2 cause blood vessels to thicken, produce inflammation in the vessel wall, and thus are regarded as "risk factors" for vascular disease, whereas ROS also act as signaling molecules in many aspects of growth factor-mediated physiological responses. Recent reports suggest that ROS play an important role in angiogenesis; however, its underlying molecular mechanisms remain unknown. Vascular endothelial growth factor (VEGF) induces angiogenesis by stimulating endothelial cell (EC) proliferation and migration primarily through the receptor tyrosine kinase VEGF receptor2 (Flk1/KDR). VEGF binding initiates tyrosine phosphorylation of KDR, which results in activation of downstream signaling enzymes including ERK1/2, Akt and eNOS, which contribute to angiogenic-related responses in EC. Importantly, the major source of ROS in EC is a NAD(P)H oxidase and EC express all the components of phagocytic NAD(P)H oxidase including gp91phox, p22phox, p47phox, p67phox and the small G protein Rac1. We have recently demonstrated that ROS derived from NAD(P)H oxidase are critically important for VEGF signaling in vitro and angiogenesis in vivo. Furthermore, a peptide hormone, angiotensin II, a major stimulus for vascular NAD(P)H oxidase, also plays an important role in angiogenesis. Because EC migration and proliferation are primary features of the process of myocardial angiogenesis, we would like to focus on the recent progress that has been made in the emerging area of NAD(P)H oxidase-derived ROS-dependent signaling in ECs, and discuss the possible roles in angiogenesis. Understanding these mechanisms may provide insight into the components of NAD(P)H oxidase as potential therapeutic targets for treatment of angiogenesis-dependent diseases such as cancer and atherosclerosis and for promoting myocardial angiogenesis in ischemic heart diseases.
血管生成是一个新血管生长的过程,它参与多种病理生理过程,如癌症、糖尿病视网膜病变和动脉粥样硬化。越来越多的证据表明,心血管疾病与血管中氧化应激增加有关。超氧化物和过氧化氢等活性氧(ROS)会导致血管增厚,在血管壁产生炎症,因此被视为血管疾病的“危险因素”,而ROS在生长因子介导的生理反应的许多方面也充当信号分子。最近的报道表明,ROS在血管生成中起重要作用;然而,其潜在的分子机制仍然未知。血管内皮生长因子(VEGF)主要通过受体酪氨酸激酶VEGF受体2(Flk1/KDR)刺激内皮细胞(EC)增殖和迁移来诱导血管生成。VEGF结合引发KDR的酪氨酸磷酸化,这导致包括ERK1/2、Akt和eNOS在内的下游信号酶的激活,这些酶有助于EC中的血管生成相关反应。重要的是,EC中ROS的主要来源是NAD(P)H氧化酶,并且EC表达吞噬性NAD(P)H氧化酶的所有成分,包括gp91phox、p22phox、p47phox、p67phox和小G蛋白Rac1。我们最近证明,源自NAD(P)H氧化酶的ROS在体外对VEGF信号传导和体内血管生成至关重要。此外,一种肽激素血管紧张素II是血管NAD(P)H氧化酶的主要刺激物,在血管生成中也起重要作用。由于EC迁移和增殖是心肌血管生成过程的主要特征,我们将重点关注EC中NAD(P)H氧化酶衍生的ROS依赖性信号传导这一新兴领域的最新进展,并讨论其在血管生成中的可能作用。了解这些机制可能有助于深入了解NAD(P)H氧化酶的成分,将其作为治疗血管生成依赖性疾病(如癌症和动脉粥样硬化)以及促进缺血性心脏病中心肌血管生成的潜在治疗靶点。