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首页> 外文会议>International Symposium on Atherosclerosis >The elastin-laminin receptor-mediated matrixdegradation. Effect of glucose concentration.Role in atherosclerosis
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The elastin-laminin receptor-mediated matrixdegradation. Effect of glucose concentration.Role in atherosclerosis

机译：弹性蛋白 - 层粘连蛋白受体介导的基质zegradation。葡萄糖浓度的影响。滴入动脉粥样硬化

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Background:We further explored the role of the elastin-laminin receptor (ELR)-mediated reactions in matrix remodeling and atherogenesis. The progressive increase of life expectancy and the increasing prevalence of diabetes type II motivated the study of the potential influence of extracellular glucose (glc) concentration on ELR-mediated oalcium homeostatic reactions as related to atherogenesis Methods: Howevermethods using cell cultures were described previously Glc-variation effects on the vessel wall were studied by tension myography on rat aorta rings and on Ca+-influx using patch clamp technology on endothelial cells Results: Previous results suggested an important role for the ELR-mediated reactions in vascular remodeling and atherogenesis Uptegulation of elastase-type endopeptidases and free-radical release plays a special role in this respect Coupling of ELR to NO-synthase (NOS) in endothelial cells results in a vasodilation which is age- and NO-dependent. This effect was shown to vanish at low (0 mM) and high (3.3 mM) [glc] in adult (6-month-old) rat aortas, but is maintained in old (30-month) aortas at the high [glc].In addition, Ca+-channel activity (Ba2 + influx) triggered by elastin peptides was maximal at normal [glc] (11 mM) and decreased at lower and higher [glc] in adult aortas High [glc] was shown also to increase elastase production and the biosynthesis of several matrix components such as collagen III and fibronectin Conclusions:Our recent results show that high [glc] is a risk factor for ELR-mediated matrix remodeling also. The maintained ELR-NOS coupling in old aortas at high [glc] should further increase ROS-production (free radical release) as shown previously. Superoxide combines with NO yielding the highly toxic peroxinitrite anion with a further increase of degrading protease production.
机译：背景：我们进一步探索了弹性蛋白 - 层蛋白受体（ELR）介导的反应在基质重塑和血管发生中的作用。预期寿命的逐步提高和糖尿病类型的普遍率促进了细胞外葡萄糖（GLC）浓度对肌钙生成方法相关的o钙稳态反应的潜在影响：然而，使用细胞培养物的方法先前GLC-通过对内皮细胞的抗弹性肌动术和Ca + -Influx对血管主动脉环和Ca + -Influx的张力肌图来研究变异效应：先前的结果表明ELR介导的血管重塑和血管发生的反应的重要作用 - 类型的内肽酶和自由基释放在这方面在内皮细胞中的偶联中起特殊作用在内皮细胞中导致血管舒张，其血液和无依赖性。显示这种效果在成人（6个月大的）大鼠主动脉的低（0mm）和高（3.3mm）[glc]下消失，但在高[GLC]的旧（30个月）主动脉中保持旧（30个月） 。此外，通过弹性蛋白肽触发的Ca + -Channel活性（Ba2 +流入）在正常的λ（11mm）下最大，并且在成年主动脉高φ中，在成年主动脉中较低，较高且较高的[glc]下降以增加弹性蛋白酶生产和生物合成的几种基质组分如胶原III和纤连蛋白的结论：我们最近的结果表明，高湿度是ELR介导的基质重塑的危险因素。在高γ的旧主动脉中保持的ELR-NOS偶联应进一步增加如前所述的ROS-生产（自由基释放）。超氧化物结合不产生高毒性过氧硝酸根阴离子，进一步增加降解蛋白酶生产。

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