Abstract
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-1β 1 Aβ42]-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.
Original language | English (US) |
---|---|
Pages (from-to) | 1731-1737 |
Number of pages | 7 |
Journal | Neurochemical Research |
Volume | 29 |
Issue number | 9 |
DOIs | |
State | Published - Sep 1 2004 |
Keywords
- Alzheimer's disease
- COX-1
- COX-2
- COX-3
- hippocampus
- human neural cells
- intron structure
- NSAIDs
ASJC Scopus subject areas
- Neuroscience(all)
- Biochemistry