title: [Myocardial expression of Spry1 and MAPK proteins of viral myocarditis].
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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Forensic Medicine, School of Biology and Basic Medical Sciences, Medical College of Soochow University, Suzhou 215123, China. whhongfei@sina.com
authors.forename: Hong-Fei
authors.initials: HF
authors.lastname: Xu
authors.forename: Lin
authors.initials: L
authors.lastname: Meng
authors.forename: Jian
authors.initials: J
authors.lastname: Yao
authors.forename: Zhen-Yong
authors.initials: ZY
authors.lastname: Gu
authors.forename: Guo-Qing
authors.initials: GQ
authors.lastname: Liu
authors.forename: Yi-Wen
authors.initials: YW
authors.lastname: Shen
authors.forename: Zi-Qin
authors.initials: ZQ
authors.lastname: Zhao
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D003384:Coxsackievirus Infections / Q000378:metabolism / Q000473:pathology; D016757:Death, Sudden, Cardiac / Q000473:pathology; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D008297:Male; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D020928:Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism*; D009205:Myocarditis / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D010750:Phosphoproteins / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011897:Random Allocation; D060888:Real-Time Polymerase Chain Reaction
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D008565:Membrane Proteins; D010750:Phosphoproteins; D012333:RNA, Messenger; C425468:Spry1 protein, mouse; D020928:Mitogen-Activated Protein Kinases