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

• Published in: Molecular medicine reports Vol. 14; no. 5; pp. 4761 - 4766
• Main Authors: Cui, Ling, He, Wen-Jing, Xu, Fan, Jiang, Li, Lv, Ming-Liang, Huang, Hui, Xu, Ji-Ping, Wu, Yu, Zhong, Hai-Bin, Zhang, Shao-Yang, Chen, Li-Fei, Shen, Chao-Lan, Yao, Gang, Li, Li, Li, Min, Zeng, Si-Ming
• Format: Journal Article
• Language: English
• Published: Greece D.A. Spandidos 01.11.2016; Spandidos Publications; Spandidos Publications UK Ltd
• Subjects: Animals; Apoptosis; Biomarkers; Biotechnology; Carrier Proteins - genetics; Carrier Proteins - metabolism; Caspase; Caspase 3 - metabolism; Caspase-3; Cellular proteins; Disease Models, Animal; DNA nucleotidylexotransferase; Gene Expression; Genetic aspects; Health aspects; HS-1-associated protein X-1; Immunofluorescence; Immunoglobulins; Injuries; Intracellular Signaling Peptides and Proteins; Ischemia; Laboratory animals; Localization; Male; Nerve Tissue Proteins - genetics; Nerve Tissue Proteins - metabolism; Nervous system; Neurological diseases; Optic nerve; optic nerve crush; Optic Nerve Injuries; Protein X; Proteins; Quantitative analysis; rat; Rats; Retina; Retina - metabolism; Retinal ganglion cells; Retinal Ganglion Cells - metabolism; Rodents; Serine-Arginine Splicing Factors - genetics; Serine-Arginine Splicing Factors - metabolism; Studies; Temperature effects; Traumatic brain injury; Western blotting; United States > US; China
• ISSN: 1791-2997; 1791-3004
• DOI: 10.3892/mmr.2016.5824

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.