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Kidney Transplantation: How Shall We Deal with Marginal Cases ? - Future Prospects from Basic Research

机译:肾脏移植:我们如何处理边缘病例? -基础研究的未来前景

摘要

The research performed at the Department of Urology Osaka University Graduate School of Medicine is overviewed. Renal ischemia-reperfusion (I/R) injury is inevitable in transplantation and is related to longterm graft function. MF-1, a bifunctional hepatocyte growth factor-macrophage stimulating protein chimera, was found to prevent apoptosis. In our study, MF-1 directly guarded cultured proximal tubular epithelial cells from hypoxia-induced necrosis and apoptosis in vitro, and MF-1 treatment ameliorated renal dysfunction by preventing apoptosis in rat I/R injury model. The erythropoietin molecule modified by carbamylation (CEPO) has been identified and was demonstrated to protect several organs without increasing the hemoglobin concentration. The therapeutic effect of CEPO was evaluated using an endothelial tube formation assay, and a rat ischemia-reperfusion injury model. CEPO treatment induced more capillarylike formation than EPO. CEPO-treated kidneys showed minimal tubular apoptosis with increased peritubular capillary endothelial cells. We identified a new therapeutic approach using CEPO to protect the kidney from ischemia-reperfusion injury by promoting angiogenesis.
机译:概述了大阪大学医学研究生院泌尿外科的研究。肾脏缺血再灌注(I / R)损伤在移植中不可避免,并且与长期移植功能有关。 MF-1是一种双功能肝细胞生长因子巨噬细胞刺激蛋白嵌合体,可防止细胞凋亡。在我们的研究中,MF-1可直接保护培养的近端肾小管上皮细胞免受缺氧引起的坏死和细胞凋亡的影响,而MF-1可通过预防大鼠I / R损伤模型中的细胞凋亡来改善肾脏功能障碍。已经鉴定出通过氨基甲酰化修饰的促红细胞生成素分子(CEPO),并被证明可以保护多个器官而不增加血红蛋白浓度。使用内皮管形成试验和大鼠缺血-再灌注损伤模型评估CEPO的治疗效果。 CEPO处理比EPO引起更多的毛细血管形成。 CEPO治疗的肾脏显示出最小的肾小管凋亡,肾小管周围毛细血管内皮细胞增加。我们确定了一种新的治疗方法,使用CEPO通过促进血管生成来保护肾脏免受缺血再灌注损伤。

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