Expression and Cell Distribution of SENP3 in Brain Tissue After Traumatic Brain Injury in Mice: A Pilot Study

• Published in: Cellular and molecular neurobiology 2015-07, Vol.35 (5), p.733-740
• Main Authors: Yu, Zhuang, Li, Hua, Yan, Hui-Ying, Yang, Yi-Qing, Zhang, Ding-Ding, Huang, Li-Tian, Xie, Guang-Bin, Liu, Ming, Tohti, Mamatemin, Hang, Chun-Hua
• Format: Article
• Language: English
• Subjects: Animals; Astrocytes - metabolism; Astrocytes - pathology; Biomedical and Life Sciences; Biomedicine; Blotting, Western; Brain - metabolism; Brain - pathology; Brain Injuries - metabolism; Brain Injuries - pathology; Caspase 3 - metabolism; Cell Biology; Cerebral Cortex - metabolism; Cerebral Cortex - pathology; Cysteine Endopeptidases; Immunohistochemistry; Male; Mice, Inbred ICR; Neurobiology; Neurons - metabolism; Neurons - pathology; Neurosciences; Original Research; Peptide Hydrolases - genetics; Peptide Hydrolases - metabolism; Pilot Projects; Real-Time Polymerase Chain Reaction; RNA, Messenger - genetics; RNA, Messenger - metabolism; Up-Regulation
• ISSN: 0272-4340; 1573-6830; 1573-6830
• DOI: 10.1007/s10571-015-0169-7

SUMO-specific proteases 3 (SENP3) is a member of the small ubiquitin-like modifier-specific protease family and deconjugates SUMO2/3 from protein substrates. To date, the expression and function of SENP3 in traumatic brain injury (TBI) are unclear. The present study examined dynamic changes in SENP3 expression in the cerebral cortex and in its cellular localization, using an acute TBI model in adult mice. SENP3 expression was examined at 3, 6, 12, 24 h, 3, and 5 days after TBI using Western Blot analysis and quantitative real-time PCR. Immunohistochemistry and immunofluorescence were examined to detect SENP3 localization. Western Blot indicated that SENP3 protein levels gradually increased from 3 h after TBI and peaked at 24 h. Quantitative real-time PCR demonstrated a gradual increase in SENP3 expression, which peaked 12 h after TBI and declined subsequently. Immunohistochemical staining demonstrated that SENP3-positive cells were observed in both the sham and 24 h post-TBI groups. However, robust expression of SENP3 was seldom observed in the sham group, while it was notably enhanced after TBI. Furthermore, immunofluorescence results revealed that the expression of SENP3 increased more significantly in neurons at day 1 after TBI compared with sham group and less significantly in astrocytes and microglia. Moreover, the SENP3-positive cells that were co-expressed with NeuN also expressed caspase-3, indicating a potential correlation between SENP3 and apoptosis after TBI. Collectively, our results showed obvious up-regulation of SENP3 expression in the brain after TBI, especially in the neurons. However, the full role of SENP3 and its therapeutic potential in TBI needs further investigation.