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Estimation of Endostatin level in pulmonary arterial hypertension patients and its relation with some parameters

机译:肺动脉高压患者内皮抑素水平的估计及其与某些参数的关系

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Biomarkers are attractive non-invasive tools for estimating and monitoring pulmonary arterial hypertension (PAH) disease and for predicting survival in patients with PAH; therefore, many studies encouraged the investigation of new biomarkers to facilitate the diagnosis of PAH. Endostatin (ES) is an endogenous inhibitor of angiogenesis. It is produced by proteolytic cleavage of the collagen XVIII that is present in both normal and cancerous tissue. In vitro examination shows that ES can manage endothelial cells (EC) physiology in ways that could influence angiogenesis. For example, solvent ES hinders EC movement and prompts improvements of the cytoskeleton that incorporate the loss of Actin stretch strands and central grips. This effect embraces restrictions on the α5β1integrins, Tropomyosin, and putative heparan sulfate proteoglycans. Consequences for the human EC cytoskeleton include Es-induced down-regulation of Mitogen-actuated Protein Kinase (MAPK), Focal Adhesion Kinase (FAK), the Urokinase Plasminogen Activator (uPA) System, and the RhoA GTPase. Human ES has likewise been shown in a few investigations to repress EC multiplication. Moreover, ES-instigated cell cycle capture in the G1 stage is joined by Cyclin D1 down-regulation. Of note, ES blocks the proliferation and organization of endothelial cells into new blood vessels, and in animal studies, ES also inhibits angiogenesis and the growth of both primary tumors and secondary metastasis. ES was initially identified by its capacity to inhibit tumor angiogenesis in vitro and also in vivo . It can also be found in both healthy and patient’ serum, and has been detected in peripheral circulation. ES could be an attractive, non-invasive prognostic marker for some diseases, notably PAH. Therefore, the presented work is aimed at investigating the ES level in blood serum as a biomarker for detection, diagnosis and early treatment of PAH patients. In doing so, the association is ascertained between gender, age, body mass index (BMI), waist circumferences, smoking, types of PAH (primary and secondary) and this potential biomarker is assessed in PAH patients.
机译:生物标记物是用于评估和监测肺动脉高压(PAH)疾病以及预测PAH患者生存率的有吸引力的非侵入性工具;因此,许多研究鼓励对新的生物标记物进行研究以促进PAH的诊断。内皮抑素(ES)是血管生成的内源性抑制剂。它是由正常组织和癌组织中都存在的胶原蛋白XVIII的蛋白水解切割产生的。体外检查显示,ES可以通过影响血管生成的方式管理内皮细胞(EC)的生理。例如,溶剂ES会阻碍EC的移动并促进细胞骨架的改善,并伴随肌动蛋白拉伸链和中央抓地力的丧失。该作用包括对α5β1整联蛋白,Tropomyosin和推定的硫酸乙酰肝素蛋白聚糖的限制。人类EC细胞骨架的后果包括Es诱导的丝裂原激活的蛋白激酶(MAPK),局灶性粘附激酶(FAK),尿激酶纤溶酶原激活剂(uPA)系统和RhoA GTPase的下调。在一些研究中同样显示出人类ES可抑制EC增殖。此外,G1期中受ES诱导的细胞周期捕获与Cyclin D1下调相关。值得注意的是,ES阻止了内皮细胞向新血管的增殖和组织,并且在动物研究中,ES还抑制了血管生成以及原发肿瘤和继发转移的生长。 ES最初是通过在体外和体内抑制肿瘤血管生成的能力来确定的。它也可以在健康和患者的血清中发现,并且已经在外周循环中被发现。 ES对于某些疾病,尤其是PAH,可能是有吸引力的,非侵入性的预后指标。因此,目前的工作旨在研究血清中的ES水平,作为检测,诊断和早期治疗PAH患者的生物标志物。通过这样做,可以确定性别,年龄,体重指数(BMI),腰围,吸烟,PAH类型(主要和次要)之间的关联,并在PAH患者中评估这种潜在的生物标志物。

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