title: Periostin as a modulator of chronic cardiac remodeling after myocardial infarction.
abstract: OBJECTIVE
  After acute myocardial infarction, during the cardiac repair phase, periostin is released into the infarct and activates signaling pathways that are essential for the reparative process. However, the role of periostin in chronic cardiac remodeling after myocardial infarction remains to be elucidated. Therefore, the objective of this study was to investigate the relationship between tissue periostin and cardiac variables in the chronic cardiac remodeling induced by myocardial infarction.
  
  
  METHODS
  Male Wistar rats were assigned to 2 groups: a simulated surgery group (SHAM; n = 8) and a myocardial infarction group (myocardial infarction; n = 13). After 3 months, morphological, functional and biochemical analyses were performed. The data are expressed as means±SD or medians (including the lower and upper quartiles).
  
  
  RESULTS
  Myocardial infarctions induced increased left ventricular diastolic and systolic areas associated with a decreased fractional area change and a posterior wall shortening velocity. With regard to the extracellular matrix variables, the myocardial infarction group presented with higher values of periostin and types I and III collagen and higher interstitial collagen volume fractions and myocardial hydroxyproline concentrations. In addition, periostin was positively correlated with type III collagen levels (r = 0.673, p = 0.029) and diastolic (r = 0.678, p = 0.036) and systolic (r = 0.795, p = 0.006) left ventricular areas. Considering the relationship between periostin and the cardiac function variables, periostin was inversely correlated with both the fractional area change (r = -0.783, p = 0.008) and the posterior wall shortening velocity (r = -0.767, p = 0.012).
  
  
  CONCLUSIONS
  Periostin might be a modulator of deleterious cardiac remodeling in the chronic phase after myocardial infarction in rats.
authors.affiliation: Universidade Estadual Paulista (UNESP), Botucatu Medical School, Internal Medicine Department, BotucatuSP, Brazil.
authors.forename: Marcos F
authors.initials: MF
authors.lastname: Minicucci
authors.forename: Priscila P dos
authors.initials: PP
authors.lastname: Santos
authors.forename: Bruna P M
authors.initials: BP
authors.lastname: Rafacho
authors.forename: Andréa F
authors.initials: AF
authors.lastname: Gonçalves
authors.forename: Lidiane P
authors.initials: LP
authors.lastname: Ardisson
authors.forename: Diego F
authors.initials: DF
authors.lastname: Batista
authors.forename: Paula S
authors.initials: PS
authors.lastname: Azevedo
authors.forename: Bertha F
authors.initials: BF
authors.lastname: Polegato
authors.forename: Katashi
authors.initials: K
authors.lastname: Okoshi
authors.forename: Elenize J
authors.initials: EJ
authors.lastname: Pereira
authors.forename: Sergio A R
authors.initials: SA
authors.lastname: Paiva
authors.forename: Leonardo A M
authors.initials: LA
authors.lastname: Zornoff
mesh_terms: D000818:Animals; D015153:Blotting, Western; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D024042:Collagen Type I / Q000032:analysis; D024061:Collagen Type III / Q000032:analysis; D003971:Diastole / Q000502:physiology; D004195:Disease Models, Animal; D006909:Hydroxyproline / Q000032:analysis; D008297:Male; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D013599:Systole / Q000502:physiology; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000502:physiology; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D015815:Cell Adhesion Molecules; D024042:Collagen Type I; D024061:Collagen Type III; C512836:Postn protein, rat; D006909:Hydroxyproline