期刊
NEUROCHEMICAL RESEARCH
卷 29, 期 9, 页码 1731-1737出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1023/B:NERE.0000035809.70905.8a
关键词
Alzheimer's disease; COX-1; COX-2; COX-3; hippocampus; human neural cells; intron structure; NSAIDs
资金
- NIA NIH HHS [AG18031] Funding Source: Medline
The cyclooxygenase ( COX) superfamily of prostaglandin synthase genes encode a constitutively expressed COX-1, an inducible, highly regulated COX-2, and a COX-3 isoform whose RNA is derived through the retention of a highly structured, G + C-rich intron 1 of the COX-1 gene. As generators of oxygen radicals, lipid mediators, and the pharmacological targets of nonsteroidal anti-inflammatory drugs ( NSAIDs), COX enzymes potentiate inflammatory neuropathology in Alzheimer's disease ( AD) brain. Because COX-2 is elevated in AD and COX-3 is enriched in the mammalian CNS, these studies were undertaken to examine the expression of COX-3 in AD and in [IL-1beta + Abeta42]-triggered human neural (HN) cells in primary culture. The results indicate that while COX-2 remains a major player in propagating inflammation in AD and in stressed HN cells, COX-3 may play ancillary roles in membrane-based COX signaling or when basal levels of COX-1 or COX-2 expression persist.
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