Noradrenaline induces expression of peroxisome proliferator activated receptor gamma (PPARγ) in murine primary astrocytes and neurons
書誌事項
- 公開日
- 2003-07-21
- 権利情報
-
- http://onlinelibrary.wiley.com/termsAndConditions#vor
- DOI
-
- 10.1046/j.1471-4159.2003.01909.x
- 公開者
- Wiley
この論文をさがす
説明
<jats:title>Abstract</jats:title><jats:p>Cerebral inflammatory events play an important part in the pathogenesis of Alzheimer's disease (AD). Agonists of the peroxisome proliferator‐activated receptor gamma (PPARγ), a nuclear hormone receptor that mediates anti‐inflammatory actions of non‐steroidal anti‐inflammatory drugs (NSAIDs) and thiazolidinediones, have been therefore proposed as a potential treatment of AD. Experimental evidence suggests that cortical noradrenaline (NA) depletion due to degeneration of the locus ceruleus (LC) – a pathological hallmark of AD – plays a permissive role in the development of inflammation in AD. To study a possible relationship between NA depletion and PPARγ‐mediated suppression of inflammation we investigated the influence of NA on PPARγ expression in murine primary cortical astrocytes and neurons. Incubation of astrocytes and neurons with 100 µ<jats:sc>m</jats:sc> NA resulted in an increase of PPARγ mRNA as well as PPARγ protein levels in both cell types. These effects were blocked by the β‐adrenergic antagonist propranolol but not by the α‐adrenergic antagonist phentolamine, suggesting that they might be mediated by β‐adrenergic receptors. Our results indicate for the first time that PPARγ expression can be modulated by the cAMP signalling pathway, and suggest that the anti‐inflammatory effects of NA on brain cells may be partly mediated by increasing PPARγ levels. Conversely, decreased NA due to LC cell death in AD may reduce endogenous PPARγ expression and therefore potentiate neuroinflammatory processes.</jats:p>
収録刊行物
-
- Journal of Neurochemistry
-
Journal of Neurochemistry 86 (4), 907-916, 2003-07-21
Wiley