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Is Increased Intracellular Calcium in Red Blood Cells a Common Component in the Molecular Mechanism Causing Anemia?

机译:红细胞中细胞内钙的增加是引起贫血的分子机制的共同组成部分吗?

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摘要

For many hereditary disorders, although the underlying genetic mutation may be known, the molecular mechanism leading to hemolytic anemia is still unclear and needs further investigation. Previous studies revealed an increased intracellular Ca2+ in red blood cells (RBCs) from patients with sickle cell disease, thalassemia, or Gardos channelopathy. Therefore we analyzed RBCs' Ca2+ content from 35 patients with different types of anemia (16 patients with hereditary spherocytosis, 11 patients with hereditary xerocytosis, 5 patients with enzymopathies, and 3 patients with hemolytic anemia of unknown cause). Intracellular Ca2+ in RBCs was measured by fluorescence microscopy using the fluorescent Ca2+ indicator Fluo-4 and subsequent single cell analysis. We found that in RBCs from patients with hereditary spherocytosis and hereditary xerocytosis the intracellular Ca2+ levels were significantly increased compared to healthy control samples. For enzymopathies and hemolytic anemia of unknown cause the intracellular Ca2+ levels in RBCs were not significantly different. These results lead us to the hypothesis that increased Ca2+ levels in RBCs are a shared component in the mechanism causing an accelerated clearance of RBCs from the blood stream in channelopathies such as hereditary xerocytosis and in diseases involving defects of cytoskeletal components like hereditary spherocytosis. Future drug developments should benefit from targeting Ca2+ entry mediating molecular players leading to better therapies for patients.
机译:对于许多遗传性疾病,尽管潜在的基因突变可能是已知的,但导致溶血性贫血的分子机制仍不清楚,需要进一步研究。先前的研究表明,镰状细胞病,地中海贫血或加多斯通道病患者的红细胞(RBC)细胞内Ca 2 + 升高。因此,我们分析了35例不同类型贫血患者(16例遗传性球血细胞增多症,11例遗传性干细胞增多症,5例酶病患者和3例未知溶血性贫血患者)中的RBCs Ca 2 + 含量原因)。使用荧光Ca 2 + 指示剂Fluo-4,通过荧光显微镜检测红细胞中的细胞内Ca 2 + ,然后进行单细胞分析。我们发现,在遗传性球细胞增多和遗传性干细胞增多症患者的红细胞中,细胞内Ca 2 + 的水平与健康对照组相比显着增加。对于未知的酶促病和溶血性贫血,红细胞中细胞内Ca 2 + 的水平没有显着差异。这些结果使我们得出这样的假设,即红血球中Ca 2 + 水平的升高是导致红血球加速从血流中清除遗传性干细胞增多症和涉及缺陷的疾病的机制中的一个共同组成部分。细胞骨架成分如遗传性球囊细胞增多症。靶向Ca 2 + 进入介导分子的分子,可以为患者带来更好的治疗方法,从而使未来的药物开发受益。

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