title: Periostin is a novel factor in cardiac remodeling after experimental and clinical unloading of the failing heart.
abstract: BACKGROUND
  Maladaptive left ventricular hypertrophy (LVH) remains a prevalent and highly morbid condition associated with end-stage heart disease. Originally evaluated in the context of bone development, periostin is important in endocardial cushion formation and has recently been implicated in heart failure. Because of its potential role in cardiovascular development, we sought to establish the role of periostin after relief of pressure overload in animal and human models.
  
  
  METHODS
  Pressure overload induction of LVH was performed by minimally invasive aortic arch banding of C57Bl6 mice. Bands were removed 1 month later to allow regression. Cardiac tissue was procured in paired samples of patients receiving LV assist devices (LVAD), with subsequent reanalysis at the time of explant for transplantation.
  
  
  RESULTS
  One week after debanding, heart weight/body weight ratios and echocardiography confirmed decreased LV mass relative to hypertrophied animals. Gene and protein expression of periostin was measured by real-time polymerase chain reaction and Western blot, and was similarly decreased compared with LVH mice. Immunohistochemical localization of periostin showed it was exclusively in the extracellular matrix of the myocardium. The decrease in periostin with pressure relief paralleled changes in interstitial fibrosis observed by picrosirius red staining. Corroborating the murine data, periostin expression was significantly reduced after LVAD-afforded pressure relief in patients.
  
  
  CONCLUSIONS
  Periostin is closely associated with pressure overload-induced LVH and LVH regression in both animal and human models. The magnitude of expression changes and the consistent nature of these changes indicate that periostin may be a mediator of cardiac remodeling.
authors.affiliation: Division of Cardiothoracic Surgery, Department of Surgery, University of North Carolina, Chapel Hill, North Carolina, USA.
authors.forename: William E
authors.initials: WE
authors.lastname: Stansfield
authors.forename: Nancy M
authors.initials: NM
authors.lastname: Andersen
authors.forename: Ru-Hang
authors.initials: RH
authors.lastname: Tang
authors.forename: Craig H
authors.initials: CH
authors.lastname: Selzman
mesh_terms: D000328:Adult; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D015153:Blotting, Western; D015815:Cell Adhesion Molecules / Q000096:biosynthesis* / Q000235:genetics; D004195:Disease Models, Animal; D018450:Disease Progression; D004452:Echocardiography; D004719:Endomyocardial Fibrosis / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D005109:Extracellular Matrix / Q000378:metabolism; D005786:Gene Expression Regulation; D006333:Heart Failure / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D016133:Polymerase Chain Reaction; D011379:Prognosis; D012313:RNA / Q000235:genetics; D017725:Ventricular Pressure / Q000502:physiology*; D020257:Ventricular Remodeling / Q000502:physiology*; D055815:Young Adult
chemical_list: D015415:Biomarkers; D015815:Cell Adhesion Molecules; C512835:POSTN protein, human; C082838:Postn protein, mouse; D012313:RNA