Upregulation of PTP1B After Rat Spinal Cord Injury

Protein tyrosine phosphatase 1B (PTP1B), a member of the protein tyrosine phosphatase family, attaches to the endoplasmic reticulum (ER) via its C-terminal tail. Previous studies have reported that PTP1B participates in various signal transduction pathways in many human diseases, including diabetes, cancers, osteoporosis, and obesity. It also plays an important role in the ER stress. ER stress induced by spinal cord injury (SCI) was reported to result in cell apoptosis. Till now, the role of PTP1B in the injury of the central nervous system remains unknown. In the present study, we built an adult rat SCI model to investigate the potential role of PTP1B in SCI. Western blot analysis detected a notable alteration of PTP1B expression after SCI. Immunohistochemistry indicated that PTP1B expressed at a low level in the normal spinal cord and greatly increased after SCI. Double immunofluorescence staining revealed that PTP1B immunoreactivity was predominantly increased in neurons following SCI. In addition, SCI resulted in a significant alteration in the level of active caspase-3, caspase-12, and 153/C/EBP homologous transcription factor protein, which were correlated with the upregulation of PTP1B. Co-localization of PTP1B/active caspase-3 was also detected in neurons. Taken together, our findings elucidated the PTP1B expression in the SCI for the first time. These results suggested that PTP1B might be deeply involved in the injury response and probably played an important role in the neuro-pathological process of SCI.