Golubnitschaja O, Wunderlich K, Decker C, Mönkemann H, Schild H H, Flammer J
Department of Radiology, University of Bonn, Germany.
Amino Acids. 2002;23(1-3):293-9. doi: 10.1007/s00726-001-0141-3.
Ocular ischemia resulting from perfusion disturbances may play a major role in initiation of glaucoma. Possibly secondary to ischemia autoimmunogenic events are activated in glaucoma patients with increased prevalence of systemic autoimmune diseases. The determination of potential molecular markers in blood leukocytes could be useful for early noninvasive diagnostics of glaucoma. Our study using subtractive hybridization showed altered gene expression in leukocytes of glaucoma patients in comparison to age and sex matched healthy subjects. Subtracted genes encoding lymphocyte IgE receptor (Fc epsilon RII/CD23), T cell-specific tyrosine kinase, thromboxan A2 receptor, alkaline phosphatase and Na(+)/K(+)-ATPase are differentially expressed in circulating leukocytes of glaucoma patients. These genes show expression profiles characteristic for adherent leukocytes which could be an important contributor to blood-brain barrier breakdown which has been found in glaucoma patients.
灌注紊乱导致的眼部缺血可能在青光眼的发病中起主要作用。在患有全身性自身免疫性疾病患病率增加的青光眼患者中,可能继发于缺血的自身免疫原性事件被激活。血液白细胞中潜在分子标志物的测定可能有助于青光眼的早期无创诊断。我们使用消减杂交的研究表明,与年龄和性别匹配的健康受试者相比,青光眼患者白细胞中的基因表达发生了改变。编码淋巴细胞IgE受体(FcεRII/CD23)、T细胞特异性酪氨酸激酶、血栓素A2受体、碱性磷酸酶和Na(+)/K(+)-ATP酶的消减基因在青光眼患者的循环白细胞中差异表达。这些基因显示出粘附白细胞特有的表达谱,这可能是青光眼患者血脑屏障破坏的一个重要因素。