Alterations in the expression of Hs1-associated protein X-1 in the rat retina after optic nerve crush

Abstract

HS-1-associated protein X-1 (Hax-1) has been suggested to be expressed in various rodent and human tissues. Accumulating evidence has demonstrated that Hax-1 exerts an anti-apoptotic effect in neurological diseases. Furthermore, it has also been reported that Hax-1 interacts with various apoptosis-associated proteins, including high temperature-regulated A2 (HtrA2) and caspase-3. Previous studies have indicated that abnormal expression of Hax-1 may be associated with the development of the nervous system and with the pathophysiology of neurological diseases, including traumatic brain injury and cerebral ischemia. The present study reported temporal-spatial patterns of Hax-1 in rat retina following optic nerve crush (ONC). Using western blotting and double-immunofluorescence, significant upregulation of Hax-1 was observed in retinal ganglion cells (RGCs) in the retina following ONC. Increased Hax-1 expression was demonstrated to be accompanied by upregulation of active-caspase-3 and HtrA2 following ONC. In addition, Hax-1 co-localized with active caspase-3 and HtrA2 in RGCs following ONC. Terminal deoxynucleotidyl transferase-mediated biotinylated-dUTP nick-end labeling staining suggested that Hax-1 was involved in RGC apoptosis following ONC. Thus, these results suggested that Hax-1 may participate in regulating RGC apoptosis via interacting with caspase-3 and HtrA2 following ONC.