期刊
NEUROREPORT
卷 20, 期 16, 页码 1500-1505出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/WNR.0b013e3283329c05
关键词
Alzheimer's disease; arachidonic acid; complement factor H; cyclooxygenase-2; cytosolic phospholipase A(2); herpes simplex virus type-1; immune response; inflammation; interleukin-1 beta; microRNA-146a
资金
- NEI NIH HHS [R01 EY006311-23, R01 EY006311-22, P30 EY002377, EY 2377, EY06311, R01 EY006311-22S1, R01 EY006311] Funding Source: Medline
- NIA NIH HHS [R01 AG018031-05S1, R01 AG018031, R01 AG023085, R01 AG038834, AG23085] Funding Source: Medline
- PHS HHS [UIO6311] Funding Source: Medline
Herpes simplex virus type-1 (HSV-1) infection of human brain cells induces changes in gene expression favorable to the propagation of the infecting agent and detrimental to the function of the host cells. We report that infection of human primary neural cells with a high phenotypic reactivator HSV-1 (117syn+) induces upregulation of a brain-enriched microRNA (miRNA)-146a that is associated with proinflammatory signaling in stressed brain cells and Alzheimer's disease. Expression of cytoplasmic phospholipase A(2), the inducible prostaglandin synthase cyclooxygenase-2, and the neuroinflammatory cytokine interleukin-1 P were each upregulated. A known miRNA-146a target in the brain, complement factor H, was downregulated. These data suggest a role for HSV-1 -induced miRNA-146a in the evasion of HSV-1 from the complement system, and the activation of key elements of the arachidonic acid cascade known to contribute to Alzheimer-type neuropathological change. NeuroReport 20:1500-1505 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据