title: [The potential effects of endoplasmic reticulum stress on the apoptosis of myocardial cells from mice with heart failure induced by acute viral myocarditis caused by B 3 Coxsackie virus].
abstract: OBJECTIVE
  To explore the apoptotic pathway mediated by endoplasmic reticulum stress in the mouse myocardium with heart failure induced by acute viral myocarditis caused by B-3 Coxsackie virus.
  
  
  METHODS
  Forty BALB/c male mice were randomly divided into 2 groups (n = 20): the control group and the virus infection group. The BALB/c mouse myocarditis was induced by B-3 Coxsackie virus and the mouse behavior was observed conventionally. All the mice were sacrificed on day 7 and the changes of left ventricular pressure (LVP) and the rate of change of left ventricular pressure (LV dp/dt) were measured. The cardiomyocytic apoptosis was analyzed by TUNEL method and the mRNA expression level of endoplasmic reticulum haperones glucose-regulated protein (GRP)78 and GRP94 was detected by RT-PCR.
  
  
  RESULTS
  (1) Compared with those of control group, the parameters of cardiac hemodynamics in the virus infection group were significantly decreased (P < 0.01); (2) Compared with that of control group, myocardial apoptosis was significantly increased in the myocardial cells from mice with heart failure induced by acute viral myocarditis (P < 0.01); (3) The mRNA expression level of GRP78 and GRP94 were increased significantly in the virus infection group compared with the control group.
  
  
  CONCLUSIONS
  These findings suggest the endoplasmic reticulum stress may mediate the apoptosis of myocardial cells in the mice myocardium of heart failure induced by acute viral myocarditis caused by B-3 Coxsackie virus.
authors.affiliation: Inner-Mongolia National University  Medical College, Tongliao, China.
authors.forename: Lei
authors.initials: L
authors.lastname: Liu
authors.forename: Hong-Jun
authors.initials: HJ
authors.lastname: Wang
authors.forename: Qing
authors.initials: Q
authors.lastname: Xin
authors.forename: Xiao-Min
authors.initials: XM
authors.lastname: Zhou
authors.forename: Ya-Jun
authors.initials: YJ
authors.lastname: Zhao
authors.forename: Xia
authors.initials: X
authors.lastname: Huang
authors.forename: Ming
authors.initials: M
authors.lastname: Zhao
mesh_terms: D000818:Animals; D017209:Apoptosis; D003384:Coxsackievirus Infections / Q000503:physiopathology*; D000091342:Endoplasmic Reticulum Chaperone BiP; D059865:Endoplasmic Reticulum Stress; D006321:Heart / Q000503:physiopathology; D006333:Heart Failure / Q000503:physiopathology / Q000821:virology*; D006360:Heat-Shock Proteins / Q000378:metabolism; D008297:Male; D008562:Membrane Glycoproteins / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D009205:Myocarditis / Q000503:physiopathology / Q000821:virology*; D009206:Myocardium / Q000473:pathology; D032383:Myocytes, Cardiac / Q000166:cytology*
chemical_list: D000091342:Endoplasmic Reticulum Chaperone BiP; D006360:Heat-Shock Proteins; C000717248:Hspa5 protein, mouse; D008562:Membrane Glycoproteins; C053387:endoplasmin