Liu Jingyu, Prell Tino, Stubendorff Beatrice, Keiner Silke, Ringer Thomas, Gunkel Anne, Tadic Vedrana, Goldhammer Nadine, Malci Ayse, Witte Otto W, Grosskreutz Julian
Hans Berger Department of Neurology, Jena University Hospital, Erlanger Allee 101, 07747 Jena, Germany.
Hans Berger Department of Neurology, Jena University Hospital, Erlanger Allee 101, 07747 Jena, Germany.
Neurosci Lett. 2016 Sep 6;630:77-83. doi: 10.1016/j.neulet.2016.07.039. Epub 2016 Jul 21.
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder associated with intracellular Ca(2+) dysregulation. The P2X receptor family is comprised of ligand-gated ion channels that respond to extracellular adenosine triphosphate (ATP) and increases permeability of calcium into the cell. The underlying mechanisms of purinergic signalling on peripheral blood mononuclear cells (PBMCs) in ALS remain unclear. Herein, we studied the expression of P2X4/P2X7 receptors and calcium homeostasis in blood cells of ALS patients.
We used PBMCs from 42 ALS patients and 19 controls. Purinergic receptors P2X4 (P2X4R) and P2X7 (P2X7R) were examined using western blot analysis. The effect of exogenous ATP on intracellular Ca(2+) homeostasis in monocytes was measured using fluorimetry by Fura-2 on a single-cell level.
Western blot analysis revealed stable P2X4R expression in patients and controls. P2X7R expression was significantly reduced (p=0.012) in ALS patients. Repetitive long-term ATP stimulation caused a sustained decrease in Ca(2+) levels in the ALS group as measured by the area under the curve, peak amplitude and peak height.
These results confirm our hypothesis that Ca(2+) abnormalities in ALS are measurable in immune cells. These findings suggest that the reduction of P2X7 receptor expression on PBMCs leads to intracellular calcium dysregulation. Our study improves the understanding of ALS pathophysiology and proposes PBMCs as a non-invasive source to study ALS.
肌萎缩侧索硬化症(ALS)是一种与细胞内钙离子调节异常相关的神经退行性疾病。P2X受体家族由配体门控离子通道组成,这些通道对细胞外三磷酸腺苷(ATP)作出反应,并增加钙离子进入细胞的通透性。ALS患者外周血单核细胞(PBMC)上嘌呤能信号传导的潜在机制仍不清楚。在此,我们研究了ALS患者血细胞中P2X4/P2X7受体的表达及钙稳态。
我们使用了42例ALS患者和19例对照的PBMC。采用蛋白质印迹分析检测嘌呤能受体P2X4(P2X4R)和P2X7(P2X7R)。通过Fura-2在单细胞水平上使用荧光测定法测量外源性ATP对单核细胞内钙离子稳态的影响。
蛋白质印迹分析显示患者和对照中P2X4R表达稳定。ALS患者中P2X7R表达显著降低(p=0.012)。通过曲线下面积、峰值幅度和峰值高度测量,重复性长期ATP刺激导致ALS组钙离子水平持续下降。
这些结果证实了我们的假设,即ALS中的钙离子异常在免疫细胞中是可测量的。这些发现表明PBMC上P2X7受体表达的降低导致细胞内钙调节异常。我们的研究增进了对ALS病理生理学的理解,并提出PBMC作为研究ALS的非侵入性来源。