title: Integrin expression during reverse remodeling in the myocardium of heart failure patients.
abstract: BACKGROUND
  The main anchoring proteins of myocardial cells with each other and with the extracellular matrix are integrins present in the membranes of myocardial cells. These integrins are important for maintaining the architecture of the myocardial tissue and the mechanotransduction in the heart. Heart failure leads to various alterations in the myocardium, such as changes in morphology, and in expression of mRNAs, miRNAs, and proteins. Left ventricular assist device (LVAD) support in heart failure patients has been described to induce reverse remodeling of the myocardium and thus to (some degree of) reversal of the aforementioned alterations. In this study, we evaluated whether changes in expression of integrins α-1, -3, -5, -6, -7, -10, -11 and β-1, -3, -5 and -6 play a role during reverse remodeling.
  
  
  METHODS
  Three-step immunoperoxidase staining procedures were applied on frozen heart tissue sections to locate the various integrins tested. Integrin mRNA expression was established by standard Q-PCR procedures.
  
  
  RESULTS
  It was shown that mRNA expression of several integrins changes significantly during LVAD support, however without subsequent changes in immunohistochemical detectable quantities. Various integrins showed different locations within the myocardium.
  
  
  CONCLUSIONS
  LVAD-induced reversed remodeling did not result in significant integrin protein expression, although changes in integrin mRNA expression suggested an adaptation to unloading.
authors.affiliation: Molecular and Immuno Pathology, Department of Pathology, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX, Utrecht, The Netherlands. h.f.j.dullens@umcutrecht.nl
authors.forename: Hub F J
authors.initials: HF
authors.lastname: Dullens
authors.forename: Marguérite E I
authors.initials: ME
authors.lastname: Schipper
authors.forename: Joyce
authors.initials: J
authors.lastname: van Kuik
authors.forename: Wendy
authors.initials: W
authors.lastname: Sohns
authors.forename: Maaike
authors.initials: M
authors.lastname: Scheenstra
authors.forename: Dick F
authors.initials: DF
authors.lastname: van Wichen
authors.forename: Matthijs F M
authors.initials: MF
authors.lastname: Van Oosterhout
authors.forename: Nicolaas
authors.initials: N
authors.lastname: de Jonge
authors.forename: Roel A
authors.initials: RA
authors.lastname: de Weger
mesh_terms: D000222:Adaptation, Physiological; D000293:Adolescent; D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D005109:Extracellular Matrix / Q000378:metabolism / Q000473:pathology; D005260:Female; D015870:Gene Expression; D006333:Heart Failure / Q000235:genetics* / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D006353:Heart-Assist Devices; D006801:Humans; D007124:Immunoenzyme Techniques; D016023:Integrins / Q000235:genetics* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D020257:Ventricular Remodeling
chemical_list: D015415:Biomarkers; D016023:Integrins