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Low O2 and high CO2 in LLC-PK1 cells culture mimics renal ischemia-induced apoptosis

机译:LLC-PK1细胞培养物中的低氧和高二氧化碳可模拟肾缺血诱导的细胞凋亡

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Ischemia, absence or loss of blood flow in organs always presents as a dual phenomenon: tissue oxygen deficit and CO2 excess (hypercapnia). Commonly hypoxic cell culture models kept CO2 at normal nonischemic values. We report a study of apoptosis in an in vitro model of renal hypoxia that mimics in vivo tissue gas atmosphere composition determined during experimental ischemia in rat kidney (low O2 plus high CO2). Renal tubular LLC-PK1 cell were transiently exposed to hypoxia, to hypercapnia or to both conditions (simulated ischemia). Exposure to simulated ischemic atmosphere, but not to low O2 or high CO2 alone, induced cell apoptosis in vitro. This suggests that ischemia-induced apoptosis in vivo would be dependent on the natural, joint action of hypoxia and hypercapnia. This should be taken into account in cell culture studies that would like to mimic in vivo ischemic conditions.
机译:器官中的缺血,缺血或血液流失始终是双重现象:组织缺氧和CO2过量(高碳酸血症)。缺氧细胞培养模型通常将CO2保持在正常的非缺血值。我们报告了在模拟大鼠肾脏缺血(低O2加高CO2)过程中确定的体内组织气体气氛组成的肾脏低氧体外模型中进行的细胞凋亡研究。肾小管LLC-PK1细胞短暂暴露于缺氧,高碳酸血症或两种情况下(模拟缺血)。暴露于模拟的局部缺血气氛,而不是单独暴露于低O2或高CO2会诱导体外细胞凋亡。这表明缺血诱导的体内细胞凋亡将取决于缺氧和高碳酸血症的自然,联合作用。在要模拟体内缺血状况的细胞培养研究中应考虑到这一点。

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