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首页> 外文期刊>Cellular Physiology and Biochemistry >Albumin and glucose effects on cell growth parameters, albumin uptake and Na+/H+-exchanger isoform 3 in OK cells
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Albumin and glucose effects on cell growth parameters, albumin uptake and Na+/H+-exchanger isoform 3 in OK cells

机译：白蛋白和葡萄糖对OK细胞中细胞生长参数，白蛋白摄取和Na + / H +交换异构体3的影响

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Background: The degree of albuminuria, the presence of sodium-dependent hypertension, and histological evidence of both tubular and interstitial pathology correlate with the progression of diabetic nephropathy. The sodium-hydrogen exchanger NHE-3 plays an integral role in both sodium reabsorption and receptor-mediated albumin endocytosis in proximal tubular cells (PTCs). The aim of this study was to investigate the direct effects of hyperglycemia and albumin on cell growth parameters, NHE-3 protein expression and albumin uptake in an in vitro model of PTCs. Methods: Opossum kidney (OK) cells were exposed to 5 mmol/l glucose (control) or 25 mmol/l (high) glucose in the presence or absence of either 0.1 or 1.0 g/l bovine serum albumin (BSA) for up to 72 hrs prior to study. 20 mmol/l mannitol + 5 mmol/l glucose was used as a control for hyperosmolality. The cell number, the degree of cell swelling, cell protein content and NHE-3 protein expression were assessed. Cellular albumin uptake and the role of NHE in both control and high glucose conditions were determined by FITC-BSA +/- NHE-inhibitor ethyl isopropyl amiloride (EIPA). Results: High glucose and the hyperosmolar control induced cellular hypertrophy, which was not modified in the presence of albumin. Cell volume was initially increased by 1.0 g/l BSA, +/-high glucose, which normalized over 4872 hrs. All experimental conditions induced an early and sustained increase in NHE-3 protein expression. High glucose increased albumin uptake, independent of changes in osmolality. EIPA reduced the albumin uptake in PTCs with kinetics supporting the role of NHE-3 in this process. Conclusion: These results suggest that exposure of PTCs to high glucose concentrations promotes osmolality mediated cell hypertrophy and increased tubular albumin reabsorption linked to an increase in NHE-3 expression. It is postulated that this increase in albumin uptake due to high glucose exposure may lead to proinflammatory protein overload of PTCs, ultimately impairing the compensatory increase in tubular albumin reabsorption. Copyright (C) 2003 S. Karger AG, Basel. [References: 34]
机译：背景：蛋白尿的程度，钠依赖性高血压的存在以及肾小管和间质病理的组织学证据与糖尿病性肾病的进展有关。钠氢交换剂NHE-3在钠重吸收和近端小管细胞（PTC）中受体介导的白蛋白内吞作用中起着不可或缺的作用。这项研究的目的是研究高血糖和白蛋白对PTCs体外模型中细胞生长参数，NHE-3蛋白表达和白蛋白摄取的直接影响。方法：在存在或不存在0.1或1.0 g / l牛血清白蛋白（BSA）的情况下，将负鼠肾（OK）细胞暴露于5 mmol / l葡萄糖（对照）或25 mmol / l（高）葡萄糖中直至研究前72小时。使用20 mmol / l甘露醇+ 5 mmol / l葡萄糖作为高渗的对照。评估细胞数量，细胞溶胀程度，细胞蛋白含量和NHE-3蛋白表达。通过FITC-BSA +/- NHE抑制剂乙基异丙基阿米洛利（EIPA）确定了细胞白蛋白的摄取以及NHE在对照和高血糖条件下的作用。结果：高葡萄糖和高渗控制引起细胞肥大，在白蛋白存在下不能改变。细胞体积最初增加1.0 g / l BSA，+ /-高葡萄糖，在4872 hrs内恢复正常。所有实验条件诱导NHE-3蛋白表达的早期和持续增加。高葡萄糖可增加白蛋白摄取，而与渗透压的变化无关。 EIPA通过动力学来支持NHE-3在此过程中的作用，从而降低了PTC中白蛋白的摄取。结论：这些结果表明，将PTC​​s暴​​露于高葡萄糖浓度下会促进重量克分子渗透压浓度介导的细胞肥大，并增加与NHE-3表达增加有关的肾小管白蛋白重吸收。假定由于高葡萄糖暴露导致白蛋白摄取的增加可能导致PTC的促炎蛋白超载，最终损害肾小管白蛋白重吸收的代偿性增加。版权所有（C）2003 S.Karger AG，巴塞尔。 [参考：34]

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