【24h】

Human amyloid-beta causes changes in the levels of endothelial protein kinase C and its alpha isoform in vitro.

机译:人淀粉样蛋白β在体外引起内皮蛋白激酶C及其α同工型水平的变化。

获取原文
获取原文并翻译 | 示例
       

摘要

Amyloid-beta (Abeta) deposits and neurofibrillary pathology are characteristic features of Alzheimer's disease (AD). The association of Abeta with cerebral vessels is an intriguing feature of AD. While there is considerable evidence of altered activities of the major isoforms of protein kinase C (PKC) in the vasculature and neurons of AD brains, little is known about the relationship between the Abeta toxicity and the altered PKC levels in cerebral endothelial cells.In this study, cultured brain endothelial cells exposed to Abeta1-40 revealed a translocation of PKC from the membrane fraction to the cytosol. The content of the isoform PKCalpha, involved in the regulation of amyloid precursor protein (APP) secretion, was decreased in the membrane-bound fraction of rat endothelial cells and increased in the cytosol after Abeta1-40 treatment. These data suggest that the accumulation of Abeta peptide in the cerebral vasculature may play a significant role in the down-regulation of PKC seen in the AD cerebral vasculature.
机译:淀粉样β(Abeta)沉积物和神经原纤维病理是阿尔茨海默氏病(AD)的特征。 Abeta与脑血管的关联是AD的有趣特征。尽管有相当多的证据表明AD大脑的脉管系统和神经元中蛋白激酶C(PKC)的主要同工型的活性发生了变化,但对Abeta毒性与脑内皮细胞中PKC水平变化之间的关系知之甚少。一项研究显示,暴露于Abeta1-40的培养的脑内皮细胞显示出PKC从膜部分转移到细胞质中。 Abeta1-40处理后,参与调节淀粉样前体蛋白(APP)分泌的同工型PKCalpha的含量在大鼠内皮细胞的膜结合部分中降低,而在细胞溶质中增加。这些数据表明,Abeta肽在脑血管中的积累可能在AD脑血管中看到的PKC的下调中起重要作用。

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