title: SCY1-like 1 binding protein 1 (SCYL1-bp1) interacts with p53-induced RING H2 protein (Pirh2) after traumatic brain injury in rats.
abstract: Traumatic brain injury (TBI) triggers a complex series of neurochemical and signaling changes that lead to neuronal dysfunction and overreactive astrocytes. In the current study, we showed that interactions between SCYL1-bp1 and Pirh2 are involved in central nervous system (CNS) injury and repair. Western blot and immunohistochemical analysis of an acute traumatic brain injury model in adult rats revealed significantly increased levels of SCYL1-bp1 and Pirh2 in the ipsilateral brain cortex, compared to contralateral cerebral cortex. Immunofluorescence double-labeling analyses further revealed that SCYL1-bp1 is mainly co-expressed with NeuN. Terminal deoxynucleotidyl transferase-mediated biotinylated-dUTP nick-end labeling staining data supported the involvement of SCYL1-bp1 and Pirh2 in neuronal apoptosis after brain injury. We additionally examined the expression profiles of active caspase-3, which were altered in correlation with the levels of SCYL1-bp1 and Pirh2. Notably, both SCYL1-bp1 and Pirh2 were colocalized with active caspase-3, and all three proteins participated in neuronal apoptosis. Immunoprecipitation experiments further revealed interactions of these proteins with each other in the pathophysiology process. To our knowledge, this is the first study to report interactions between SCYL1-bp1 and Pirh2 in traumatic brain. Our data collectively indicate that SCYL1-bp1 and Pirh2 play important roles in CNS pathophysiology after TBI.
authors.affiliation: Department of Neurology, Surgical Comprehensive Laboratory, Affiliated Hospital of Nantong University, 19 Qi-Xiu Road, Nantong, Jiangsu 226001, People's Republic of China.
authors.forename: Jian
authors.initials: J
authors.lastname: Chen
authors.forename: Feihui
authors.initials: F
authors.lastname: Zou
authors.forename: Hongran
authors.initials: H
authors.lastname: Fu
authors.forename: Hui
authors.initials: H
authors.lastname: Mao
authors.forename: Mingjie
authors.initials: M
authors.lastname: Gong
authors.forename: Lanchun
authors.initials: L
authors.lastname: Ni
authors.forename: Xide
authors.initials: X
authors.lastname: Xu
authors.forename: Jinlong
authors.initials: J
authors.lastname: Shi
authors.forename: Kaifu
authors.initials: K
authors.lastname: Ke
authors.forename: Maohong
authors.initials: M
authors.lastname: Cao
authors.forename: Fei
authors.initials: F
authors.lastname: Zhou
authors.forename: Wei
authors.initials: W
authors.lastname: Shi
mesh_terms: D033942:Adaptor Proteins, Vesicular Transport / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D034961:Antigens, Nuclear / Q000235:genetics / Q000378:metabolism; D017209:Apoptosis / Q000235:genetics; D001253:Astrocytes / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D001930:Brain Injuries / Q000378:metabolism*; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D002493:Central Nervous System Diseases / Q000235:genetics / Q000378:metabolism*; D002540:Cerebral Cortex / Q000378:metabolism; D008297:Male; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism; D009474:Neurons / Q000378:metabolism; D054730:Protein Interaction Domains and Motifs; D051381:Rats; D017207:Rats, Sprague-Dawley; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism*; D044767:Ubiquitin-Protein Ligases / Q000235:genetics / Q000378:metabolism*; D015854:Up-Regulation
chemical_list: D033942:Adaptor Proteins, Vesicular Transport; D034961:Antigens, Nuclear; D015415:Biomarkers; D002352:Carrier Proteins; D009419:Nerve Tissue Proteins; C546339:Rbfox3 protein, rat; C531983:Scyl1 protein, rat; D016159:Tumor Suppressor Protein p53; C577621:Rchy1 protein, rat; D044767:Ubiquitin-Protein Ligases; D053148:Caspase 3