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The role of TNF-α in renal tubular cell damage following exposure to pathological conditions in vitro

机译：TNF-α在体外接触病理条件下肾小管细胞损伤中的作用

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In humans, intravesical pressures exceeding 40 cm H{sub}2O are associated with upper urinary tract deterioration and vesicoureteral reflux [McGuire et al., 1981]; if these elevated pressures persist over time, they may eventually lead to kidney failure. Evidence provided by animal models [Fung and Atala, 1998] and clinical findings [Carr et al., 1991] imply that kidney damage and/or failure following bladder outlet obstruction may be the result of elevated hydrostatic pressure within the kidney (a consequence of increased bladder pressures and urine reflux) and/or renal cell hypoxia (resulting from decreased blood flow to the kidney). Although irreversible alterations in kidney function following bladder outlet obstruction have been observed in both animal models and clinically, the effects of hydrostatic pressure and hypoxia (applied in a manner which simulates in viva conditions) on renal function, as well as the mechanism(s) behind these responses, have not been well investigated at the cellular level. This study, therefore, will use a novel in vitro model to expose kidney tubular epithelial cells to either sustained hydrostatic pressures of 60 cm H20 (a pressure level which is known to induce kidney damage), or to hypoxia, or to both conditions simultaneously. Select cell functions, such as expression of N-Acetyl-β-D-glucosaminidase （NAG; an indicator of kidney cell damage), cell apoptosis, and the synthesis of Tumor Necrosis Factor-u (TNF-α; a growth factor which is known to be involved in renal tubular cell apoptosis [Soler et al., 1999]) will be monitored following exposure of renal tubular cells to these mechanical stimuli.
机译：在人类中，膀胱内压超过40cm {sub} 2o与上部尿路劣化和vesicoureteral回流相关[麦格尔等，1981];如果这些升高的压力随着时间的推移持续存在，它们最终可能导致肾衰竭。动物模型[Fung和Atala，1998]和临床发现[Carr等人，1991]提供的证据意味着膀胱出口梗阻后肾脏损伤和/或失败可能是肾脏内静水压力升高的结果（其后果增加膀胱压力和尿液回流）和/或肾细胞缺氧（由肾脏的血流降低而导致）。虽然在膀胱出口障碍物后，在两只动物模型和临床上观察到肾功能不可逆转的改变，但临床上，静水压力和缺氧的影响（以血管条件模拟的方式）对肾功能，以及机制在这些反应后面，在细胞水平上没有得到很好的研究。因此，该研究将使用新的体外模型将肾小管上皮细胞暴露于60cm H20（已知肾脏损伤的压力水平）或缺氧的持续静水压压力，或同时发生。选择细胞功能，例如N-乙酰-β-D-葡糖胺酶的表达（NAG;肾细胞损伤的指标），细胞凋亡和肿瘤坏死因子-U的合成（TNF-α;已知参与肾小管细胞凋亡的生长因子[Soler等，1999]）将是在肾小管细胞暴露于这些机械刺激后监测。

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