Alterations in the Expression of the Anti-Apoptotic Factor HAX-1 upon Seizures-Induced Hippocampal Injury in the Neonatal Rat Brain |
| |
Authors: | A Rami M Kim J Niquet A Langhagen |
| |
Institution: | (1) Institut f?r Zellul?re und Molekulare Anatomie (Anatomie III), Klinikum der Johann Wolfgang von Goethe-Universit?t, Theodor-Stern-Kai 7, 60590 Franfurt/Main, Germany;(2) Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA;(3) Dr. Senckenbergische Anatomie, Anatomie III, Universit?tsklinikum, Theodor-Stern-Kai 7, 60590 Frankfurt/Main, Germany |
| |
Abstract: | HS1-associated protein X1 (HAX-1) is a mitochondrial protein which interacts with a diverse group of molecules such as inflammatory
cytokines; interleukin-1, hematopoietic lineage specific protein-1 and vimentin. It has been reported that HAX-1 may act as
antiapoptotic protein in HeLa- and Jurkat cells after Fas-treatment, irradiation or serum deprivation. This underlines the
evidence that HAX-1 might be involved in both receptor- and mitochondria-mediated apoptosis pathways. However, the role of
HAX-1 in neuronal death induced by status epilepticus in the immature brain has not been reported. In this study, we performed
a status epilepticus in rats and investigated the dynamic changes of HAX-1 expression, HtrA2 distribution and caspase-3 activation
in the hippocampus. Western blot and immunohistochemistry analysis revealed that HAX-1 was expressed at very low levels in
the hippocampus. Status epilepticus in the immature brain significantly induced increased cytosolic accumulation of HAX-1
in a biphasic manner, induced an upregulation of HtrA2 and enhanced caspase-3 activity in the selectively vulnerable hippocampal
CA1-subfield. Taken together, these results suggested that HAX-1 is probably involved in the pathophysiology of cell death
induced by epilepsy. |
| |
Keywords: | |
本文献已被 PubMed SpringerLink 等数据库收录! |
|