ABSTRACT
OBJECTIVE@#To discuss the myocardial expression of Spry1 and MAPK proteins of viral myocarditis (VMC), to reveal its mechanism of sudden death, and to provide guides for forensic identification of sudden cardiac death.@*METHODS@#Thirty Balb/c male mice were randomly divided into VMC group and control group, inoculated intraperitoneally with Coxsackievirus B3 and Eagel's solution, respectively. After the mice were sacrificed, the cardiac tissues of the mice were taken to proceed regular pathological examination. The changes of Spry1 protein, Spry1 mRNA and MAPK protein were detected by immunohistochemistry, Western blotting and real-time PCR.@*RESULTS@#Under light microscope, the pathologic changes included myocardial interstitial edema, inflammatory cells infiltration, myocardial necrosis, and focal and patchy necrosis of myocardial fiber in VMC group. The expression of Spry1 protein in VMC group was lower than that in control group (P < 0.05). There was slightly decreased expression of Spry1 of the mRNA level in VMC group (P > 0.05). But the MAPK protein expression in VMC group was higher than that in control group (P < 0.05).@*CONCLUSION@#The pathway of MAPK/ERK involving Spry1 protein accelerates the expression of collagen, which may contribute to arrhythmia, heart failure and even sudden cardiac death.
Subject(s)
Animals , Male , Mice , Adaptor Proteins, Signal Transducing/metabolism , Coxsackievirus Infections/pathology , Death, Sudden, Cardiac/pathology , Disease Models, Animal , Immunohistochemistry , Membrane Proteins/metabolism , Mice, Inbred BALB C , Mitogen-Activated Protein Kinases/metabolism , Myocarditis/virology , Myocardium/pathology , Phosphoproteins/metabolism , RNA, Messenger/metabolism , Random Allocation , Real-Time Polymerase Chain ReactionABSTRACT
OBJECTIVE@#In order to improve accuracy and reliability of forensic diagnosis of sudden cardiac death, pathogenesis and relationship between the viral myocarditis (VMC) and dilated cardiomyopathy (DCM) were investigated.@*METHODS@#Improved immunohistochemical technique was used to detect the expression of the CAR in myocardium samples, including 22 deceased with VMC, 20 deceased with DCM and 16 control deceased.@*RESULTS@#The brown staining on the cell membrane of myocardium showed positive result. There was a prominent CAR expression in VMC group and DCM group, which were statistically significant difference compared with control group (P < 0.05).@*CONCLUSION@#The CAR expression showed significantly higher in VMC and DCM groups. The viral infection can result in myocardial necrosis and impaired cardiac functions. These abnormalities can trigger a cascade of events that contributed to the progress of VMC to DCM.
Subject(s)
Female , Humans , Male , Cardiomyopathy, Dilated/pathology , Case-Control Studies , Coxsackie and Adenovirus Receptor-Like Membrane Protein , Coxsackievirus Infections/complications , Death, Sudden, Cardiac , Forensic Pathology , Immunohistochemistry , Myocarditis/virology , Myocardium/pathology , Receptors, Virus/metabolism , Staining and LabelingABSTRACT
OBJECTIVE@#In order to improve the accuracy and reliability in sudden cardiac death, the pathogenesis and relationship between the viral myocarditis and dilated cardiomyopathy were investigated.@*METHODS@#Improved immunohistochemical technique was adopted to detect the expression of the dystrophin in myocardium from 25 viral myocarditis, 28 dilated cardiomyopathy and 17 control cases including normal, coronary atherosclerotic heart disease and hypertension heart disease as control.@*RESULTS@#The positive rate of dystrophin protein expression in control group was 100%, that in viral myocarditis was 88%, and that in dilated cardiomyopathy was 57%, There were significant differences among three groups (P<0.05), and the correlation between viral myocarditis and dilated cardiomyopathy group (r = -0.526)were also found.@*CONCLUSION@#The myocardial cytoskeletal protein is disrupted in viral myocarditis and dilated cardiomyopathy, and the dystrophin protein may be involved in the pathogenesis of viral myocarditis and dilated cardiomyopathy. The viral infect and impair heart functions by cleaving host dystrophin proteins may ultimately contributes to the viral myocarditis to the converting from dilated cardiomyopathy.