RESUMO
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.