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Recombinant Human MG53 Mediated Protection against Injury to Neuronal Cells
Author(s) -
Paleo Brian J,
Madalena Kathryn,
Mital Rohan,
Bodnar Tom,
Rose Aubrey,
McElha Kevin,
Lerch Jessica,
Weisleder Noah
Publication year - 2019
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.2019.33.1_supplement.848.2
Subject(s) - microbiology and biotechnology , skeletal muscle , biology , regeneration (biology) , myocyte , nervous system , cell , neuroscience , anatomy , biochemistry
Injuries to the nervous system can cause irreversible damage to mental and motor function. This has led to extensive interest in studying mechanisms of neuronal regeneration and recovery from injury. Since many neurons are terminally differentiated, increasing the emphasis on maintaining cell survival could provide more translational potential for treatment of neuronal diseases and injuries. While several cell types are known to survive injury through plasma membrane repair mechanisms, there has been little investigation of membrane repair in neurons and even fewer efforts to target membrane repair in diseases affecting neurons. Much of the current understanding of the plasma membrane repair response comes from studies of these repair processes in striated muscle cells. Studies from our laboratory group and others demonstrated that mitsugumin 53 (MG53), a muscle‐enriched tripartite motif (TRIM) family protein also known as TRIM72, is an essential component of the cell membrane repair machinery in skeletal muscle, cardiac muscle, liver, and alveolar epithelial cells. Interestingly, recombinant human MG53 (rhMG53) when applied exogenously can increase membrane repair and integrity both in vitro and in vivo . Increasing the membrane repair capacity of neurons could potentially minimize the death of these cells and affect the progression of various neuronal diseases. While there have been previous studies of membrane repair mechanisms in skeletal muscles that are relevant to neurotrauma, there has been little investigation of membrane repair specifically in neurons. While the action of rhMG53 has been proven to be robust, lack of knowledge of membrane repair in the nervous system leads to questions of the potential efficacy of membrane repair in neurons. In this study we assess the therapeutic potential of rhMG53 in the treatment of various traumatic neuropathies. We find a robust repair response exists in various neuronal cells and that rhMG53 can increase neuronal membrane repair in vitro and in vivo . These findings provide novel, direct evidence of conserved membrane repair responses in neurons and that these repair mechanisms can be targeted as a potential therapeutic approach for the treatment of neuronal injury. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .