title: Differential protein expression and basal lamina remodeling in human heart failure.
abstract: A goal of this study was to identify and investigate previously unrecognized components of the remodeling process in the progression to heart failure by comparing protein expression in ischemic failing (F) and nonfailing (NF) human hearts.
  
  
  
  Protein expression differences were investigated using multidimensional protein identification and validated by Western analysis. This approach detected basal lamina (BL) remodeling, and further studies analyzed samples for evidence of structural BL remodeling. A rat model of pressure overload (PO) was studied to determine whether nonischemic stressors also produce BL remodeling and impact cellular adhesion.
  
  
  
  Differential protein expression of collagen IV, laminin α2, and nidogen-1 indicated BL remodeling develops in F versus NF hearts Periodic disruption of cardiac myocyte BL accompanied this process in F, but not NF heart. The rat PO myocardium also developed BL remodeling and compromised myocyte adhesion compared to sham controls.
  
  
  
  Differential protein expression and evidence of structural and functional BL alterations develop during heart failure. The compromised adhesion associated with this remodeling indicates a high potential for dysfunctional cellular integrity and tethering in failing myocytes. Therapeutically targeting BL remodeling could slow or prevent the progression of heart disease.
authors.affiliation: Department of Surgery, University of Michigan, Ann Arbor, MI, USA.
authors.forename: Evelyn H
authors.initials: EH
authors.lastname: Kim
authors.affiliation: Department of Surgery, University of Michigan, Ann Arbor, MI, USA.
authors.forename: Vladimir I
authors.initials: VI
authors.lastname: Galchev
authors.affiliation: Korea Basic Science Institute, Ochang, Korea.
authors.forename: Jin Young
authors.initials: JY
authors.lastname: Kim
authors.affiliation: Department of Cardiac Surgery, University of Michigan, Ann Arbor, MI, USA.
authors.forename: Sean A
authors.initials: SA
authors.lastname: Misek
authors.affiliation: Department of Cardiac Surgery, University of Michigan, Ann Arbor, MI, USA.
authors.forename: Tamara K
authors.initials: TK
authors.lastname: Stevenson
authors.affiliation: Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.
authors.forename: Matthew D
authors.initials: MD
authors.lastname: Campbell
authors.affiliation: Department of Cardiac Surgery, University of Michigan, Ann Arbor, MI, USA.
authors.forename: Francis D
authors.initials: FD
authors.lastname: Pagani
authors.affiliation: Cardiovascular Division, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
authors.forename: Sharlene M
authors.initials: SM
authors.lastname: Day
authors.affiliation: DNA Sequencing and Microarray Facility, University of Michigan, Ann Arbor, MI, USA.
authors.forename: T Craig
authors.initials: TC
authors.lastname: Johnson
authors.affiliation: DNA Sequencing and Microarray Facility, University of Michigan, Ann Arbor, MI, USA.
authors.forename: Joseph G
authors.initials: JG
authors.lastname: Washburn
authors.affiliation: Cardiovascular Division, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
authors.forename: Karen L
authors.initials: KL
authors.lastname: Vikstrom
authors.affiliation: Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.|Cardiovascular Division, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
authors.forename: Daniel E
authors.initials: DE
authors.lastname: Michele
authors.affiliation: Department of Surgery, University of Michigan, Ann Arbor, MI, USA.
authors.forename: David E
authors.initials: DE
authors.lastname: Misek
authors.affiliation: Department of Cardiac Surgery, University of Michigan, Ann Arbor, MI, USA.|Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.
authors.forename: Margaret V
authors.initials: MV
authors.lastname: Westfall
mesh_terms: D000368:Aged; D000818:Animals; D001485:Basement Membrane / Q000378:metabolism* / Q000473:pathology; D024141:Collagen Type IV / Q000235:genetics* / Q000378:metabolism; D004195:Disease Models, Animal; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D006333:Heart Failure / Q000175:diagnosis* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007797:Laminin / Q000235:genetics* / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000235:genetics* / Q000378:metabolism; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000175:diagnosis* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D061251:Primary Cell Culture; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D024141:Collagen Type IV; D007797:Laminin; D008562:Membrane Glycoproteins; C102645:laminin alpha 2; C029967:nidogen
keywords: Basal lamina; Heart failure; Myocardium; Proteins; Remodeling