title: [Role of cyclic adenosine monophosphate response element binding protein in ventricular pacing induced cardiac electrical remodeling in a canine model].
abstract: OBJECTIVE
  This project is designed to explore the potential role of cyclic adenosine monophosphate (cAMP) response element binding protein (CREB) in cardiac electrical remodeling induced by pacing at different ventricular positions in dogs.
  
  
  METHODS
  An animal model by implanting the pacemakers in beagles was established. According to the different pacing positions, the animals were divided into 4 groups:conditional control group (n=6), left ventricle pacing group (n=6), right ventricle pacing group (n=6) and bi-ventricle pacing group (n=6). Cardiac and electrical remodeling were observed by echocardiography, electrocardiogram and plasma BNP. Myocardial pathology and protein expression of extracellular regulated protein kinases1/2 (ERK1/2), P38 mitogen activated protein kinases (P38 MAPK) and CREB were examined at 4 weeks post pacing.
  
  
  RESULTS
  Cardiac structure and plasma BNP level were similar among 4 groups (all P>0.05). Electrocardiogram derived Tp-Te interval was significantly prolonged post pacing (92±11, 91±10, and 79±13 ms vs. 60±12 ms), and the Tp-Te interval in bi-ventricle pacing group was shorter than in left or right ventricle pacing group (P < 0.05). Western blot results showed that the expression of p-ERK1/2 in left ventricular myocardium of left ventricle pacing group, right ventricular myocardium of right ventricle pacing group and bi-ventricular myocardium of bi-ventricle pacing group was 2.7±0.4, 2.4±0.2, 1.7±0.1 and 1.9±0.2, respectively, the expression of p-P38 MAPK was 1.9±0.3, 1.7±0.2, 0.8±0.1 and 1.1±0.1, respectively, and the expression of p-CREB was 2.1±0.2, 2.0±0.2, 2.7±0.4 and 2.6±0.3, respectively. The p-ERK1/2 and p-P38 MAPK expression of bi-ventricle pacing group was lower,but the p-CREB expression was higher compared to the other pacing groups (P < 0.05).
  
  
  CONCLUSIONS
  Ventricular pacing could induce electrical remodeling evidenced by prolonged Tp-Te interval and increased phosphorylation of ERK1/2 and p38 MAPK and reduced phosphorylation of CREB. Compared with single ventricle pacing, bi-ventricle pacing could attenuate electrical remodeling in this model.
authors.affiliation: Department of Cardiology, Second Hospital Affiliated to Wenzhou Medical University, Wenzhou 325000, China.
authors.forename: Xuesi
authors.initials: X
authors.lastname: Chen
authors.affiliation: Department of Cardiology, Second Hospital Affiliated to Wenzhou Medical University, Wenzhou 325000, China.
authors.forename: Xingxing
authors.initials: X
authors.lastname: Chen
authors.affiliation: Department of Cardiology, Second Hospital Affiliated to Wenzhou Medical University, Wenzhou 325000, China.
authors.forename: Junhua
authors.initials: J
authors.lastname: Cheng
authors.affiliation: Department of Cardiology, Second Hospital Affiliated to Wenzhou Medical University, Wenzhou 325000, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Hong
authors.affiliation: Department of Cardiology, Second Hospital Affiliated to Wenzhou Medical University, Wenzhou 325000, China.
authors.forename: Cheng
authors.initials: C
authors.lastname: Zheng
authors.affiliation: Department of Cardiology, Second Hospital Affiliated to Wenzhou Medical University, Wenzhou 325000, China.
authors.forename: Jinglin
authors.initials: J
authors.lastname: Zhao
authors.affiliation: Department of Cardiology, Second Hospital Affiliated to Wenzhou Medical University, Wenzhou 325000, China.
authors.forename: Jin
authors.initials: J
authors.lastname: Li
authors.affiliation: Department of Cardiology, Second Hospital Affiliated to Wenzhou Medical University, Wenzhou 325000, China; Email: linjiafeng@medmail.com.cn.
authors.forename: Jiafeng
authors.initials: J
authors.lastname: Lin
mesh_terms: D000249:Adenosine Monophosphate / Q000378:metabolism*; D000818:Animals; D064752:Atrial Remodeling / Q000502:physiology*; D015153:Blotting, Western; D002304:Cardiac Pacing, Artificial; D004285:Dogs; D004452:Echocardiography; D004562:Electrocardiography; D006352:Heart Ventricles; D009206:Myocardium; D010766:Phosphorylation; D020218:Response Elements; D020257:Ventricular Remodeling; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism*
chemical_list: D000249:Adenosine Monophosphate; D048051:p38 Mitogen-Activated Protein Kinases