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Membrane repair protein Mitsugumin 53 as a potential therapeutic for the treatment of traumatic brain injury
Author(s) -
Moloughney Joseph Gennaro,
Alloush Jenna,
LeHoang Oanh,
Weisleder Noah Lucas
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.803.8
Subject(s) - traumatic brain injury , medicine , in vivo , brain damage , neuroscience , biology , psychiatry , microbiology and biotechnology
Traumatic brain injury (TBI) is an injury to the brain generated from an external mechanical force causing temporary or permanent impairment of physical and cognitive functions. The Centers for Disease Control and Prevention (CDC) estimates that TBI is a factor in a third of all injury‐related deaths in the United States, accounting for approximately 50,000 deaths annually. Research has shown that injury to neuronal cell membranes is a significant contributing factor in the progression of TBI, therefore targeting membrane repair represents a novel therapeutic strategy for the treatment of traumatic brain injuries. Mitsugumin 53 (MG53) is a TRIM family protein and an essential component of the cell membrane repair machinery. Our research group has shown that MG53 can increase the membrane resealing capability of neuronal cells following mechanical injury in vitro and that recombinant human MG53 (rhMG53) can be delivered to the injury site and minimize damage in the brain following TBI in vivo . Histological examination of brain tissue isolated from mice pretreated with rhMG53 and subjected to TBI display a significant decrease in cleaved caspase‐3 and Fluoro‐Jade C staining at the injury site, suggesting reduction in cell death due to enhanced membrane repair. In addition, motor coordination was improved in mice pretreated with rhMG53 compared to saline control as measured by the rotarod performance test after TBI. Our results show that rhMG53 can mitigate neuronal death and damage brought on by TBI and provide a protective effect in an in vivo mouse model. Research was funded by the National Football League (NFL) Charities.