The serum of dysautonomia patients enhances proliferation and signaling in Schwann cells.
The serum of dysautonomia patients enhances proliferation and signaling in Schwann cells.
复制标题
自主神经功能障碍患者的血清增强雪旺细胞的增殖和信号传导。
DOI：
10.1016/j.neulet.2009.10.083
复制
发表时间：
2010
影响因子：
2.5
通讯作者：
Berti-Mattera,LilianaN
中科院分区：
文献类型：
--
作者：
Lambrecht,ReinH;Pollard,KatherineA;Alshekhlee,Amer;Chelimsky,ThomasC;Berti-Mattera,LilianaN
自主神经系统疾病或自主神经功能障碍影响很大一部分人口，特别是妇女，并代表了诊断的挑战。植物神经紊乱的生物标志物的鉴定，以及随后的筛查方法的发展，将有利于诊断和症状管理。我们研究了来自15名特征明确的自主神经功能障碍患者（平均年龄49±16岁，10名女性，5名男性）和10名对照受试者（平均年龄31±14岁，5名女性，5名男性）的血清对培养的雪旺细胞增殖和这些细胞中的促分裂原活化蛋白激酶（MAPK）活性的影响。我们将患者的特征与对细胞增殖和信号传导的影响相关联。总体而言，我们观察到一个显着增加的增殖时，雪旺细胞与女性自主神经功能障碍患者的血清孵育时，与对照组和男性患者相比。有趣的是，IgG的去除显著降低了患者血清的增殖作用。我们还观察到与男性和女性患者血清孵育后p38 MAPK的显著活化。这些结果表明，患者血清中含有有助于异常雪旺细胞增殖和信号传导的因子，并可能最终导致自主神经功能障碍。我们的观察结果代表了一个有希望的第一步，在确定植物神经功能障碍的生物标志物。
Disorders of the autonomic nervous system, or dysautonomias, affect a large segment of the population, especially women, and represent a diagnostic challenge. Identification of biomarkers for autonomic disorders, and the subsequent development of screening methods, would benefit diagnosis and symptom management. We studied the effect of sera from fifteen well-characterized dysautonomia patients (mean age 49±16 years, 10 females, 5 males) and ten control subjects (mean age 31±14 years, 5 females, 5 males) on the proliferation of cultured Schwann cells and activity of mitogen-activated protein kinases (MAPKs) in these cells. We correlated characteristics of patients with the effects on cell proliferation and signaling. Overall, we observed a significant increase in proliferation when Schwann cells were incubated with sera from female dysautonomia patients when compared to control subjects and male patients. Interestingly, removal of IgGs significantly reduced the proliferative effect of patient sera. We also observed significant activation of p38 MAPK following incubation with both male and female patient sera. These results suggest that patient sera contain factors that contribute to aberrant Schwann cell proliferation and signaling and may ultimately lead to autonomic nerve dysfunction. Our observations represent a promising first step in the identification of dysautonomia biomarkers.