title: Time course of atrial fibrillation-induced cellular structural remodeling in atria of the goat.
abstract: BACKGROUND
  Previously we documented cellular structural changes of a non-degenerative nature in atrial myocytes after atrial fibrillation (AF) in the goat. The time course of these changes was not studied.
  
  
  RESULTS
  Cellular structural changes were studied by light- and electron microscopy and immunohistochemistry in goat atria after 0-16 weeks AF. The first sign of cellular structural remodeling was a more homogeneous chromatin distribution, at 1 week of AF. Sub-structural changes in mitochondria and sarcoplasmic reticulum occurred gradually. Cellular degeneration was absent. The degree of myolysis and glycogen accumulation increased till 8 weeks of AF and did not increase further from thereon. After 16 weeks of AF, 42% of the myocytes in the right atrial free wall were affected by myolysis. The diameter of the atrial myocytes increased. Dedifferentiation of the atrial myocytes was suggested by altered expression patterns of structural proteins, such as the disappearance of cardiotin (1 week), the A-I junctional part of titin (4 weeks), desmin at the intercalated disk (ID) (8 weeks) and a gradual re-expression of alpha-smooth muscle actin.
  
  
  CONCLUSIONS
  Remodeling of the cellular ultrastructure in atrial myocardium of the goat develops progressively during AF. Re-expression of fetal proteins indicate dedifferentiation of atrial myocytes, analogous to observations in hibernating myocardium of the ventricle.
authors.affiliation: Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands. jannie.ausma@fys.unimaas.nl
authors.forename: J
authors.initials: J
authors.lastname: Ausma
authors.forename: N
authors.initials: N
authors.lastname: Litjens
authors.forename: M H
authors.initials: MH
authors.lastname: Lenders
authors.forename: H
authors.initials: H
authors.lastname: Duimel
authors.forename: F
authors.initials: F
authors.lastname: Mast
authors.forename: L
authors.initials: L
authors.lastname: Wouters
authors.forename: F
authors.initials: F
authors.lastname: Ramaekers
authors.forename: M
authors.initials: M
authors.lastname: Allessie
authors.forename: M
authors.initials: M
authors.lastname: Borgers
mesh_terms: D000185:Actinin / Q000378:metabolism; D000199:Actins / Q000378:metabolism; D000818:Animals; D001281:Atrial Fibrillation / Q000378:metabolism / Q000503:physiopathology*; D015815:Cell Adhesion Molecules / Q000378:metabolism; D048429:Cell Size; D064211:Connectin; D003238:Connective Tissue / Q000000981:diagnostic imaging; D004195:Disease Models, Animal; D006041:Goats; D006325:Heart Atria / Q000000981:diagnostic imaging* / Q000378:metabolism* / Q000473:pathology; D009124:Muscle Proteins / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000378:metabolism; D011494:Protein Kinases / Q000378:metabolism; D011506:Proteins / Q000378:metabolism*; D013997:Time Factors; D014463:Ultrasonography
chemical_list: D000199:Actins; D015815:Cell Adhesion Molecules; D064211:Connectin; D009124:Muscle Proteins; D011506:Proteins; C104594:cardiotin; D000185:Actinin; D011494:Protein Kinases