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

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 Hax­1 exerts an anti­apoptotic effect in neurological diseases. Furthermore, it has also been reported that Hax­1 interacts with various apoptosis­associated proteins, including high temperature-regulated A2 (HtrA2) and caspase­3. Previous studies have indicated that abnormal expression of Hax­1 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 temporal­spatial patterns of Hax­1 in rat retina following optic nerve crush (ONC). Using western blotting and double­immunofluorescence, significant upregulation of Hax­1 was observed in retinal ganglion cells (RGCs) in the retina following ONC. Increased Hax­1 expression was demonstrated to be accompanied by upregulation of active­caspase­3 and HtrA2 following ONC. In addition, Hax-1 co­localized with active caspase­3 and HtrA2 in RGCs following ONC. Terminal deoxynucleotidyl transferase­mediated biotinylated-dUTP nick­end labeling staining suggested that Hax­1 was involved in RGC apoptosis following ONC. Thus, these results suggested that Hax­1 may participate in regulating RGC apoptosis via interacting with caspase­3 and HtrA2 following ONC.