Many hepatocellular activities may be proximally regulated by intracellular signalling proteins including mitogen-activated protein kinases (MAPK). In this study, signalling events from epidermal growth factor (EGF) and insulin were examined in primary cultured human and rat hepatocytes. Using Weste
Activation of mitogen activated protein kinase (MAPK) pathways after soman poisoning in rat cerebellar granule neurons
✍ Scribed by J. Pejchal; J. Österreicher; J. Kassa; A. Tichý; J. Mokrý
- Publisher
- John Wiley and Sons
- Year
- 2008
- Tongue
- English
- Weight
- 75 KB
- Volume
- 28
- Category
- Article
- ISSN
- 0260-437X
- DOI
- 10.1002/jat.1323
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
The expression of activated p38 mitogen‐activated protein kinase (MAPK) and activated MAPK transcription factors c‐jun, c‐myc and elk‐1 were examined in rat cerebellum after soman poisoning to determine the pathogenetic mechanism of the non‐specific long‐term effects of nerve agents. Male Wistar rats were poisoned by intramuscular administration of soman at a dose 60 µg kg^−1^ (70% LD~50~) and samples were taken 1, 7 and 14 days after poisoning, immunohistochemically stained and p‐p38MAPK, p‐c‐jun, p‐c‐myc and p‐elk‐1 expressions were measured using image analysis. Control groups were administered with saline instead of soman. The expression of activated p38MAPK and c‐myc increased 14 days after soman poisoning while c‐jun and elk‐1 expressions remained unchanged 1, 7 and 14 days after soman poisoning. Delayed activation of p38 MAPK and its targets might be involved in the pathogenetic mechanism of the long‐term neurophysiological toxic effects of nerve agents. Copyright © 2007 John Wiley & Sons, Ltd.
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