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MG53 reduces cell death associated with hemorrhagic shock ischemia/reperfusion (I/R) injury by increasing membrane repair capacity
Author(s) -
Moloughney Joseph Gennaro,
Hersey John,
Tan Tao,
Hsai Henry,
Weisleder Noah
Publication year - 2012
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.26.1_supplement.1001.3
Subject(s) - lactate dehydrogenase , creatine kinase , reperfusion injury , ischemia , programmed cell death , medicine , apoptosis , shock (circulatory) , pathology , andrology , biology , biochemistry , enzyme
Physical trauma is a leading cause of death in the United States. While interventions to restore blood pressure and volume following acute trauma are essential, the abrupt restoration of blood flow following ischemia results in significant cell damage and death. As a result, injury caused by a hemorrhagic shock ischemia/reperfusion (I/R) event can have severe consequences, including organ failure and patient death. MG53 is a TRIM family protein which is an essential component of the cell membrane repair machinery in cardiac and skeletal muscle. Following various types of membrane damage, including injury associated with I/R, our research group has shown that MG53 facilitates formation of a membrane repair patch to restore the integrity of the disrupted membrane. Creatine kinase (CK) and lactate dehydrogenase (LDH) assays revealed significantly increased membrane resealing capacity in cultured mammalian cells or isolated mg53 −/− flexor digitorum brevis (FDB) muscle fibers in the presence of rhMG53. Histological examination of tissue isolated from mice pretreated with rhMG53 and subjected to hemorrhagic shock reveal a significant decrease in Evan's blue dye staining in multiple tissues, suggesting reduction in necrotic cell death due to enhanced membrane repair. Our results show that recombinant human MG53 (rhMG53) can serve a protective role and mitigate cellular death and damage brought on by I/R following hemorrhagic shock. Research was funded by the Foundation for UMDNJ.