首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >EXPRESSION OF LACTOFERRIN RECEPTORS IS INCREASED IN THE MESENCEPHALON OF PATIENTS WITH PARKINSON DISEASE
【24h】

EXPRESSION OF LACTOFERRIN RECEPTORS IS INCREASED IN THE MESENCEPHALON OF PATIENTS WITH PARKINSON DISEASE

机译:帕金森氏病患者的间充质中乳铁蛋白受体的表达增加

获取原文
获取原文并翻译 | 示例
           

摘要

The degeneration of nigral dopaminergic neurons in Parkinson disease is believed to be associated with oxidative stress, Since iron levels are increased in the substantia nigra of parkinsonian patients and this metal catalyzes the formation of free radicals, it may be involved in the mechanisms of nerve cell death, The cause of nigral iron increase is not understood, Iron acquisition by neurons may occur from iron-transferrin complexes with a direct interaction with specific membrane receptors, but recent results have shown a tow density of transferrin receptors in the substantia nigra. To investigate whether neuronal death in Parkinson disease may be associated with changes in a pathway supplementary to that of transferrin, lactoferrin (lactotransferrin) receptor expression was studied in the mesencephalon, In this report we present evidence from immunohistochemical staining of postmortem human brain tissue that lactoferrin receptors are localized on neurons (perikarya, dendrites, axons), cerebral microvasculature, and, in some cases, glial cells, In parkinsonian patients, lactoferrin receptor immunoreactivity on neurons and microvessels was increased and more pronounced in those regions of the mesencephalon where the loss of dopaminergic neurons is severe, Moreover, in the substantia nigra, the intensity of immunoreactivity on neurons and microvessels was higher for patients with higher nigral dopaminergic loss. These data suggest that lactoferrin receptors on vulnerable neurons may increase intraneuronal iron levels and contribute to the degeneration of nigral dopaminergic neurons in Parkinson disease. [References: 48]
机译:帕金森病中的黑色素多巴胺能神经元的退化被认为与氧化应激有关。由于帕金森氏症患者黑质中铁的含量增加,并且该金属催化自由基的形成,因此它可能参与了神经细胞的机制。死亡,黑色素铁增加的原因尚不清楚,神经元铁的摄取可能来自与特定膜受体直接相互作用的铁转铁蛋白复合物,但最近的结果显示黑质中转铁蛋白受体的丝束密度。为了研究帕金森氏病的神经元死亡是否可能与转铁蛋白途径的改变有关,在中脑中研究了乳铁蛋白(乳酸转铁蛋白)受体的表达。在本报告中,我们提供了从人死后脑组织的免疫组织化学染色得到的证据受体位于神经元(perikarya,树突,轴突),大脑微脉管系统,在某些情况下位于神经胶质细胞。在帕金森病患者中,神经元和微血管上的乳铁蛋白受体免疫反应性增加,在中脑的那些区域中更为明显多巴胺能神经元的严重受损,此外,在黑质中,对黑质多巴胺能损失较高的患者,神经元和微血管的免疫反应强度较高。这些数据表明,易损神经元上的乳铁蛋白受体可能会增加神经内神经铁水平,并有助于帕金森病中的黑色素多巴胺能神经元的变性。 [参考:48]

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号