Neurochemical Research

, Volume 37, Issue 1, pp 116–125

Alterations in the Expression of the Anti-Apoptotic Factor HAX-1 upon Seizures-Induced Hippocampal Injury in the Neonatal Rat Brain

Original Paper

DOI: 10.1007/s11064-011-0589-9

Cite this article as:
Rami, A., Kim, M., Niquet, J. et al. Neurochem Res (2012) 37: 116. doi:10.1007/s11064-011-0589-9


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.


HAX-1SeizuresCell deathStatus epilepticus

Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  1. 1.Institut für Zelluläre und Molekulare Anatomie (Anatomie III), Klinikum der Johann Wolfgang von Goethe-UniversitätFranfurt/MainGermany
  2. 2.Department of NeurologyDavid Geffen School of Medicine at UCLALos AngelesUSA
  3. 3.Dr. Senckenbergische Anatomie, Anatomie III, UniversitätsklinikumFrankfurt/MainGermany