Role of transcription factors in mediating post-ischemic cerebral inflammation and brain damage

Inflammation is a known precipitator of neuronal death after cerebral ischemia. The mechanisms that promote or curtail the start and spread of inflammation in brain are still being debated. By virtue of their capability to modulate gene expression, several transcription factors induced in the ischem...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Neurochemistry international 2007-06, Vol.50 (7), p.1014-1027
Hauptverfasser: Yi, Jae-Hyuk, Park, Seung-Won, Kapadia, Ramya, Vemuganti, Raghu
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Inflammation is a known precipitator of neuronal death after cerebral ischemia. The mechanisms that promote or curtail the start and spread of inflammation in brain are still being debated. By virtue of their capability to modulate gene expression, several transcription factors induced in the ischemic brain can modulate the post-ischemic inflammation. While the induction of transcription factors such as IRF1, NF-κB, ATF-2, STAT3, Egr1 and C/EBPβ is thought to promote post-ischemic inflammation, activation of transcription factors such as HIF-1, CREB, c-fos, PPARα, PPARγ and p53 is thought to prevent post-ischemic inflammation and neuronal damage. Of these, PPARγ which is a ligand-activated transcription factor was recently shown to prevent inflammatory gene expression in several animal models CNS disorders. This review article discusses some of the molecular mechanisms of PPARγ induction by its agonists following focal cerebral ischemia.
ISSN:0197-0186
1872-9754
DOI:10.1016/j.neuint.2007.04.019