title: The Role of Uncoupling Protein 2 During Myocardial Dysfunction in a Canine Model of Endotoxin Shock.
abstract: To explore the role of uncoupling protein 2 (UCP2) during myocardial dysfunction in a canine model of endotoxin shock, 26 mongrel canines were randomly divided into the following four groups: A (control group; n = 6), B2 (shock after 2 h; n = 7), B4 (shock after 4 h; n = 7), and B6 (shock after 6 h; n = 6). Escherichia coli endotoxin was injected into the canines via the central vein, and hemodynamics were monitored. Energy metabolism, UCP2 mRNA and protein expression, and UCP2 localization were analyzed, and the correlation between energy metabolism changes, and UCP2 expression was determined. After the canine endotoxin shock model was successfully established, the expression of UCP2 mRNA and protein was found to increase, with later time points showing significant increases (P < 0.05). Immunofluorescence assays of UCP2 in heart tissue showed that UCP2 was localized in the cytoplasm, and its expression pattern was the same as that found in the mRNA and protein analyses. The energy metabolism results revealed that the ADP levels increased, but the ATP and phosphocreatine (PCr) levels and ATP/ADP and PCr/ATP ratios decreased in the model. In particular, the PCr/ATP ratio was significantly different from that of the control group 6 h after shock (P < 0.05). Furthermore, correlation analysis showed that the UCP2 protein and mRNA levels were negatively correlated with myocardial energy levels. In summary, decreased energy synthesis can occur in the myocardium during endotoxin shock, and UCP2 may play an important role in this process. The negative correlation between UCP2 expression and energy metabolism requires further study, as the results might contribute to the treatment of sepsis with heart failure.
authors.affiliation: *Department of Critical Care Medicine, Peking Union Medical College Hospital; and †Department of Critical Care Medicine, Dalian Central Hospital, Beijing, China.
authors.forename: Xiaoting
authors.initials: X
authors.lastname: Wang
authors.forename: Dawei
authors.initials: D
authors.lastname: Liu
authors.forename: Wenzhao
authors.initials: W
authors.lastname: Chai
authors.forename: Yun
authors.initials: Y
authors.lastname: Long
authors.forename: Longxiang
authors.initials: L
authors.lastname: Su
authors.forename: Rongli
authors.initials: R
authors.lastname: Yang
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D004195:Disease Models, Animal; D004285:Dogs; D004734:Energy Metabolism; D005260:Female; D007150:Immunohistochemistry; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism*; D008297:Male; D024101:Mitochondrial Proteins / Q000235:genetics / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D010725:Phosphocreatine / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012772:Shock, Septic / Q000235:genetics / Q000378:metabolism*; D000071246:Uncoupling Protein 2
chemical_list: D007473:Ion Channels; D024101:Mitochondrial Proteins; D012333:RNA, Messenger; D000071246:Uncoupling Protein 2; D010725:Phosphocreatine; D000255:Adenosine Triphosphate