)| PMID |
17901552 ( ) |
|---|---|
| Title | Function of COX-2 and prostaglandins in neurological disease. |
| Abstract | Induction of COX-2 expression and enzymatic activity promotes neuronal injury in a number of models of neurological disease. Inhibition of COX-2 activity, either genetically or pharmacologically, has been shown to be neuroprotective in rodent models of stroke, Parkinson's disease, and amyotrophic lateral sclerosis. Inhibition of COX activity with nonsteroidal anti-inflammatory drugs (NSAIDs) reduces inflammation and amyloid accumulation in murine transgenic models of Familial Alzheimer's disease, and the use of NSAIDs decreases the risk of developing Alzheimer's disease in healthy aging populations. COX-mediated neuronal injury is presumed be due to downstream effects of one or more prostaglandin products including PGE2, PGD2, PGF2alpha, PGI2 (prostacylin) and TXA2 (thromboxane) that effect cellular changes through activation of specific prostaglandin receptor subtypes and second messenger systems. In this proceeding, we review recent data demonstrating effects of prostaglandin signaling on neuronal viability that are paradoxically protective, when taken in the context that COX-2 induces neuronal injury in the setting of excitotoxicity. Conversely, in the context of an inflammatory stimulus, the EP2 receptor enhances neuronal injury. These findings argue for an additional level of complexity in the prostaglandin response in neurological disease. N. Wolfe Street, Baltimore, MD 21205, USA. |
NOTE: Color highlight is limited to the abstract and SciMiner text-mining mode. If you see much more identified targets below from "Targets by SciMiner Summary" and "Targets by SciMiner Full list", they may have been identified from the full text.
Targets by SciMiner Summary
| HUGO ID | Symbol | Target Name | #Occur | ActualStr |
|---|---|---|---|---|
| 9605 | PTGS2 | prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase) | 10 | COX | COX-2 | COX-mediated | cox 2 | |
| 9592 | PTGDS | prostaglandin D2 synthase 21kDa (brain) | 1 | PGD2 | |
| 620 | APP | amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease) | 1 | amyloid | |
| 9600 | PTGFR | prostaglandin F receptor (FP) | 1 | prostaglandin receptor | |
| 9594 | PTGER2 | prostaglandin E receptor 2 (subtype EP2), 53kDa | 1 | EP2 | |
Targets by SciMiner Full list
| HUGO ID | Symbol | Name | ActualStr | Score | FlankingText |
|---|---|---|---|---|---|
| 9605 | PTGS2 | prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase) | COX-2 | 1.0 | Function of COX-2 and prostaglandins in neurological disease |
| 9605 | PTGS2 | prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase) | COX-2 | 1.0 | Induction of COX-2 expression and enzymatic activity promotes neuronal injury in a number |
| 9605 | PTGS2 | prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase) | COX-2 | 1.0 | Inhibition of COX-2 activity either genetically or pharmacologically has been shown to be |
| 620 | APP | amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease) | amyloid | 1.0 | activity with nonsteroidal anti-inflammatory drugs (NSAIDs) NSAIDs reduces inflammation and amyloid accumulation in murine transgenic models of Familial Alzheimer's disease and |
| 9605 | PTGS2 | prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase) | COX | 0.0 | Inhibition of COX activity with nonsteroidal anti-inflammatory drugs (NSAIDs) NSAIDs reduces inflammation and |
| 9592 | PTGDS | prostaglandin D2 synthase 21kDa (brain) | PGD2 | 1.3 | downstream effects of one or more prostaglandin products including PGE2 PGD2 PGF2alpha PGI2 (prostacylin) prostacylin and TXA2 (thromboxane) thromboxane that effect |
| 9605 | PTGS2 | prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase) | COX-mediated | 0.0 | COX-mediated neuronal injury is presumed be due to downstream effects of |
| 9605 | PTGS2 | prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase) | COX-2 | 1.0 | that are paradoxically protective when taken in the context that COX-2 induces neuronal injury in the setting of excitotoxicity |
| 9594 | PTGER2 | prostaglandin E receptor 2 (subtype EP2), 53kDa | EP2 | 0.6 | Conversely in the context of an inflammatory stimulus the EP2 receptor enhances neuronal injury |
| 9605 | PTGS2 | prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase) | cox 2 | 1.0 | function of cox 2 and prostaglandins in neurological disease. |
| 9605 | PTGS2 | prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase) | cox 2 | 1.0 | induction of cox 2 expression and enzymatic activity promotes neuronal injury in a number of models of neurological disease. |
| 9605 | PTGS2 | prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase) | cox 2 | 1.0 | inhibition of cox 2 activity either genetically or pharmacologically has been shown to be neuroprotective in rodent models of stroke parkinson's disease and amyotrophic lateral sclerosis. |
| 9600 | PTGFR | prostaglandin F receptor (FP) | prostaglandin receptor | 1.0 | umed be due to downstream effects of one or more prostaglandin products including pge2 pgd2 pgf2alpha pgi2 prostacylin and txa2 thromboxane that effect cellular changes through activation of specific prostaglandin receptor subtypes and second messenger systems. |
| 9605 | PTGS2 | prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase) | cox 2 | 1.0 | in this proceeding we review recent data demonstrating effects of prostaglandin signaling on neuronal viability that are paradoxically protective when taken in the context that cox 2 induces neuronal injury in the setting of excitotoxicity. |