...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Potential role of the formyl peptide receptor-like 1 (FPRL1) in inflammatory aspects of Alzheimer's disease.
【24h】

Potential role of the formyl peptide receptor-like 1 (FPRL1) in inflammatory aspects of Alzheimer's disease.

机译：甲酰肽受体样1（FPRL1）在阿尔茨海默氏病炎症方面的潜在作用。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Alzheimer's disease (AD) is a progressive, neurodegenerative disease characterized by the presence of multiple senile plaques in the brain tissue, which are also associated with considerable inflammatory infiltrates. Although the precise mechanisms of the pathogenesis of AD remain to be determined, the overproduction and precipitation of a 42 amino acid form of beta amyloid (Abeta(42)) in plaques have implicated Abeta in neurodegeneration and proinflammatory responses seen in the AD brain. Our recent studies revealed that the activation of formyl peptide receptor-like 1 (FPRL1), a seven-transmembrane, G-protein-coupled receptor, by Abeta(42) may be responsible for accumulation and activation of mononuclear phagocytes (monocytes and microglia). We further found that upon binding FPRL1, Abeta(42) was rapidly internalized into the cytoplasmic compartment in the form of Abeta(42)/FPRL1 complexes. Persistent exposure of FPRL1-expressing cells to Abeta(42) resulted in intracellular retention of Abeta(42)/FPRL1 complexes and the formation of Congo-red-positive fibrils in mononuclear phagocytes. Our observations suggest that FPRL1 may not only mediate the proinflammatory activity of Abeta(42) but also actively participate in Abeta(42) uptake and the resultant fibrillar formation. Therefore, FPRL1 may constitute an additional molecular target for the development of therapeutic agents for AD.
机译：阿尔茨海默氏病（AD）是一种进行性神经退行性疾病，其特征在于脑组织中存在多个老年斑，这些斑块也与大量炎症浸润有关。尽管AD发病机理的确切机制尚待确定，但斑块中42个氨基酸形式的β淀粉样蛋白（Abeta（42））的过量生产和沉淀已暗示Abeta参与了AD脑中的神经变性和促炎反应。我们最近的研究表明，Abeta（42）对甲酰肽受体样1（FPRL1）的激活（七跨膜，G蛋白偶联受体）可能是单核吞噬细胞（单核细胞和小胶质细胞）的积累和激活的原因。 。我们进一步发现，结合FPRL1后，Abeta（42）便以Abeta（42）/ FPRL1复合物的形式迅速内化到细胞质区室中。 FPRL1表达细胞持续暴露于Abeta（42）导致Abeta（42）/ FPRL1复合物的细胞内滞留并在单核吞噬细胞中形成刚果红阳性原纤维。我们的观察结果表明，FPRL1不仅可以介导Abeta（42）的促炎活性，而且还可以积极参与Abeta（42）的摄取和由此产生的原纤维形成。因此，FPRL1可能构成开发AD治疗药物的其他分子靶标。

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