title: Down-regulation of sarcolipin mRNA expression in chronic atrial fibrillation.
abstract: BACKGROUND
  Abnormal intracellular Ca2+ homeostasis is an important modulator of chronic atrial fibrillation. Sarcolipin, a homologue of phospholamban, is specifically expressed in the atria, and may play an important role in modulating intracellular Ca2+ homeostasis in the atria. The aim of this study was to investigate the expression of sarcolipin mRNA in the atrial myocardium of patients with chronic atrial fibrillation.
  
  
  METHODS
  We analyzed the expression of sarcolipin, phospholamban, cardiac calsequestrin and sodium calcium exchanger mRNAs in the right atrial myocardium from nine patients with mitral valvular disease with atrial fibrillation (MVD/AF), nine patients with MVD who had normal sinus rhythm (MVD/NSR), and 10 control patients with normal sinus rhythm who received open heart surgery (controls). The expression of mRNA was measured using the ABI PRISM 7700 Sequence Detection System (Applied Biosystems, Foster City, CA).
  
  
  RESULTS
  Relative expression levels of sarcolipin mRNA were significantly lower in MVD/AF (0.60 +/- 0.11) than in either MVD/NSR (1.28 +/- 0.17, P < 0.01) or controls (1.10 +/- 0.10, P < 0.05). The expression levels of sarcolipin mRNA were significantly lower in the group with high values for right atrial pressure. The expression levels of phospholamban, cardiac calsequestrin and sodium calcium exchanger mRNAs were comparable among all three groups.
  
  
  CONCLUSIONS
  Chronic electrical and mechanical overload decreased the expression of sarcolipin mRNA in the right atrial myocardium in patients with chronic atrial fibrillation. Down-regulation of sarcolipin mRNA may be part of atrial fibrillation-induced atrial remodelling.
authors.affiliation: Department of Physiology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Uemura
authors.forename: T
authors.initials: T
authors.lastname: Ohkusa
authors.forename: K
authors.initials: K
authors.lastname: Hamano
authors.forename: M
authors.initials: M
authors.lastname: Nakagome
authors.forename: H
authors.initials: H
authors.lastname: Hori
authors.forename: M
authors.initials: M
authors.lastname: Shimizu
authors.forename: M
authors.initials: M
authors.lastname: Matsuzaki
authors.forename: S
authors.initials: S
authors.lastname: Mochizuki
authors.forename: S
authors.initials: S
authors.lastname: Minamisawa
authors.forename: Y
authors.initials: Y
authors.lastname: Ishikawa
mesh_terms: D000328:Adult; D000368:Aged; D001281:Atrial Fibrillation / Q000209:etiology / Q000235:genetics*; D002135:Calcium-Binding Proteins / Q000235:genetics; D002155:Calsequestrin / Q000235:genetics; D002908:Chronic Disease; D015536:Down-Regulation / Q000235:genetics; D005260:Female; D015870:Gene Expression / Q000235:genetics; D006325:Heart Atria / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D008944:Mitral Valve Insufficiency / Q000150:complications / Q000235:genetics; D008946:Mitral Valve Stenosis / Q000150:complications / Q000235:genetics; D009124:Muscle Proteins / Q000235:genetics*; D009206:Myocardium / Q000378:metabolism; D011510:Proteolipids / Q000235:genetics*; D012333:RNA, Messenger / Q000032:analysis*; D019831:Sodium-Calcium Exchanger / Q000235:genetics; D000099211:Phospholamban
chemical_list: D002135:Calcium-Binding Proteins; D002155:Calsequestrin; D009124:Muscle Proteins; D011510:Proteolipids; D012333:RNA, Messenger; D019831:Sodium-Calcium Exchanger; D000099211:Phospholamban; C077258:sarcolipin