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Physiological concept for a blood based CFTR test

机译：基于血液的CFTR测试的生理概念

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We tested the hypothesis that the cystic fibrosis transmembrane conductance regulator ( CFTR) could be involved in the volume regulation of human red blood cells (RBC). Experiments were based on two gadolinium (Gd3+) sensitive mechanisms, i.e. inhibition of ATP release (theta ATP(i)) and membrane destabilization. RBC of either cystic fibrosis (CF) patients or healthy donors (non-CF) were exposed to KCl buffer containing Gd3+. A significantly larger quantity of non-CF RBC (2.55 %) hemolyzed as compared to CF RBC (0.89 %). It was found that both of the Gd3+ mechanisms simultaneously are needed to achieve hemolysis, since either overriding theta ATP(i) by exogenous ATP addition prevented Gd3+ induced hemolysis, or mimicking theta ATP(i) by apyrase in absence of Gd3+ could not trigger hemolysis. Additionally, ion driven volume uptake was found to be a prerequisite for Gd3+ induced hemolysis as chloride and potassium channel blockers reduced the Gd3+ response. The results show that in non-CF RBC Gd3+ exerts its dual effect leading to hemolysis. On the contrary, in CF RBC, lacking CFTR dependent ATP release, the sole Gd3+ effect of membrane destabilization is not sufficient to induce hemolysis similar to non-CF. This concept could form the basis of a novel method suitable for testing CFTR function in a blood sample. Copyright (c) 2006 S. Karger AG, Basel.
机译：我们检验了以下假设：囊性纤维化跨膜电导调节剂（CFTR）可能参与人类红细胞（RBC）的体积调节。实验基于两种g（Gd3 +）敏感机制，即抑制ATP释放（θATP（i））和膜不稳定。囊性纤维化（CF）患者或健康供体（非CF）的RBC暴露于含有Gd3 +的KCl缓冲液中。与CF RBC（0.89％）相比，大量非CF RBC（2.55％）被溶血。已发现实现溶血同时需要同时使用两种Gd3 +机制，因为通过外源ATP添加来覆盖theta ATP（i）可以阻止Gd3 +诱导的溶血，或者在没有Gd3 +的情况下通过腺苷三磷酸酶模拟theta ATP（i）不会触发溶血。 。此外，发现离子驱动的体积摄取是Gd3 +诱导溶血的先决条件，因为氯化物和钾通道阻滞剂降低了Gd3 +反应。结果表明，在非CF RBC中，Gd3 +发挥其双重作用导致溶血。相反，在缺乏CFTR依赖的ATP释放的CF RBC中，与非CF相似，膜去稳定作用的唯一Gd3 +效应不足以诱导溶血。该概念可以构成适用于测试血液样本中CFTR功能的新方法的基础。版权所有（c）2006 S.Karger AG，巴塞尔。

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