title: Alterations in gene expression of proteins involved in the calcium handling in patients with atrial fibrillation.
abstract: BACKGROUND
  Atrial fibrillation (AF) leads to a loss of atrial contraction within hours to days. During persistence of AF, cellular dedifferentiation and hypertrophy occur, eventually resulting in degenerative changes and cell death. Abnormalities in the calcium handling in response to tachycardia-induced intracellular calcium overload play a pivotal role in these processes.
  
  
  RESULTS
  The purpose was to investigate the mRNA expression of proteins and ion channels influencing the calcium handling in patients with persistent AF. Right atrial appendages were obtained from 18 matched controls in sinus rhythm (group 1) and 18 patients with persistent AF undergoing elective cardiac surgery. Previous duration of AF was < or = 6 months in 9 (group 2) and > 6 months in 9 patients (group 3). In a single semiquantitative polymerase chain reaction, the mRNA of interest and of glyceraldehyde-3-phosphate dehydrogenase, were coamplified and separated by gel electrophoresis. L-type calcium channel alpha1 subunit mRNA content was inversely related to the duration of AF: -26% in group 2 compared to group 1 (P = 0.2), and -49% in group 3 compared to group 1 (P = 0.01). Inhibitory guanine nucleotide binding protein ialpha2 mRNA content was reduced in group 3 compared to group 1 (-30%, P = 0.01). Sarcoplasmic reticulum calcium ATPase, phospholamban and sodium-calcium exchanger mRNA contents were not affected by AF.
  
  
  CONCLUSIONS
  AF-induced alterations in mRNA contents of proteins and ion channels involved in the calcium handling seem to occur in relation to the previous duration of AF. In the present patient population, these changes were significant only if AF lasted > 6 months.
authors.affiliation: Department of Cardiology, Thoraxcenter, University Hospital Groningen, The Netherlands. i.c.van.gelder@thorax.azg.nl
authors.forename: I C
authors.initials: IC
authors.lastname: Van Gelder
authors.forename: B J
authors.initials: BJ
authors.lastname: Brundel
authors.forename: R H
authors.initials: RH
authors.lastname: Henning
authors.forename: A E
authors.initials: AE
authors.lastname: Tuinenburg
authors.forename: R G
authors.initials: RG
authors.lastname: Tieleman
authors.forename: L
authors.initials: L
authors.lastname: Deelman
authors.forename: J G
authors.initials: JG
authors.lastname: Grandjean
authors.forename: P J
authors.initials: PJ
authors.lastname: De Kam
authors.forename: W H
authors.initials: WH
authors.lastname: Van Gilst
authors.forename: H J
authors.initials: HJ
authors.lastname: Crijns
mesh_terms: D000368:Aged; D001281:Atrial Fibrillation / Q000235:genetics* / Q000378:metabolism; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000235:genetics*; D002135:Calcium-Binding Proteins / Q000235:genetics; D000252:Calcium-Transporting ATPases / Q000235:genetics*; D017931:DNA Primers / Q000737:chemistry; D018076:DNA, Complementary / Q000096:biosynthesis; D005260:Female; D005500:Follow-Up Studies; D015870:Gene Expression; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000096:biosynthesis; D012519:Sarcoplasmic Reticulum / Q000378:metabolism; D019831:Sodium-Calcium Exchanger / Q000235:genetics; D000099211:Phospholamban
chemical_list: D002118:Calcium; D015220:Calcium Channels; D002135:Calcium-Binding Proteins; D000252:Calcium-Transporting ATPases; D017931:DNA Primers; D018076:DNA, Complementary; D012333:RNA, Messenger; D019831:Sodium-Calcium Exchanger; D000099211:Phospholamban