Open AccessCorrelation between connexin and traumatic brain injury in patients
Author(s) -
Chen Bonian,
Sun Liwei,
Wu Xiaozhe,
Ma Jun
Publication year - 2017
Publication title -
brain and behavior
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.915
H-Index - 41
ISSN - 2162-3279
DOI - 10.1002/brb3.770
Subject(s) - connexin , traumatic brain injury , medicine , protein kinase a , disease , kinase , glasgow coma scale , mapk/erk pathway , gap junction , neuroscience , animal studies , bioinformatics , pathology , biology , psychiatry , microbiology and biotechnology , intracellular
Abstract Background Identification of molecular alterations of damaged tissue in patients with neurological disorders can provide novel insight and potential therapeutic target for treatment of the diseases. It has been suggested by animal studies that connexins (CXs), a family of gap junction proteins, could contribute to neuronal cell death and associate with neurological deficits during trauma‐induced damage. Nevertheless, whether specific CXs are involved in traumatic brain injury ( TBI ) has remained unexplored in human patients. Methods In a clinical setting, we performed a correlation study of 131 TBI patients who received brain surgery. CXs (including CX40, CX43, and CX45) were examined in the harvested brain tissues for studying the relationships with the Glasgow Coma Scale scores of the patients. Results Specifically, the protein levels of CX43 (negatively) and CX40 (positively) are associated with the extent of disease severity. Meanwhile, the phosphorylation status of CX43 was strongly associated with the severe TBI patients who contain relatively high kinase activities of PKC (protein kinase C) and MAPK (mitogen‐activated protein kinase), two possible activators for CX43 phosphorylation. Conclusion These data highlight that a cluster of connexin family gap junction proteins not previously studied in humans is significantly correlated with the disease progression of TBI .