Document Detail


Periostin is a novel factor in cardiac remodeling after experimental and clinical unloading of the failing heart.
MedLine Citation:
PMID:  19932262     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
William E Stansfield; Nancy M Andersen; Ru-Hang Tang; Craig H Selzman
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Annals of thoracic surgery     Volume:  88     ISSN:  1552-6259     ISO Abbreviation:  Ann. Thorac. Surg.     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-11-25     Completed Date:  2010-01-05     Revised Date:  2014-09-19    
Medline Journal Info:
Nlm Unique ID:  15030100R     Medline TA:  Ann Thorac Surg     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  1916-21     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Adult
Animals
Biological Markers / metabolism
Blotting, Western
Cell Adhesion Molecules / biosynthesis*,  genetics
Disease Models, Animal
Disease Progression
Echocardiography
Endomyocardial Fibrosis / etiology,  metabolism,  pathology
Extracellular Matrix / metabolism
Gene Expression Regulation
Heart Failure / etiology,  metabolism*,  physiopathology
Heart Ventricles / metabolism,  physiopathology*,  ultrasonography
Humans
Hypertrophy, Left Ventricular / complications*,  metabolism,  physiopathology
Immunohistochemistry
Male
Mice
Mice, Inbred C57BL
Myocardium / metabolism,  pathology
Polymerase Chain Reaction
Prognosis
RNA / genetics
Ventricular Pressure / physiology*
Ventricular Remodeling / physiology*
Young Adult
Grant Support
ID/Acronym/Agency:
R01 HL089592/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Cell Adhesion Molecules; 0/POSTN protein, human; 0/Postn protein, mouse; 63231-63-0/RNA
Comments/Corrections
Comment In:
Ann Thorac Surg. 2009 Dec;88(6):1921-2   [PMID:  19932263 ]

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