title: Sarcoplasmic reticulum Ca2+ regulatory protein gene expression in human right atrium under hemodynamic overload.
abstract: Sarcoplasmic reticulum (SR) Ca2+-adenosine triphosphatase (ATPase) mRNA expression is reduced in the failing human myocardium. However, it is not known whether SR Ca2+-regulatory protein gene expression is altered in human myocardial tissue subjected to pressure overload or volume overload. We sought to determine whether SR Ca2+-regulatory protein gene expression is altered in human atrial tissue subjected to mechanical overload. We obtained right atrial myocardial tissue (about 250mg) at open-heart surgery from three groups of patients: no hemodynamic overload to the right atrium (control group; 12 patients), atrial septal defect (ASD group; 8 patients), and tricuspid regurgitation (TR group; 7 patients). We measured the myocyte size, the area of interstitial fibrosis, SR Ca2+,-ATPase, and ryanodine receptor mRNA abundance. The isolated cardiocyte area and the percent area of interstitial fibrosis were in the order TR > ASD > control (P < 0.05). The SR Ca2+-ATPase mRNA level in TR was significantly decreased (P = 0.004) compared with the control, whereas in the ASD group it did not differ significantly from control. There were no significant differences in ryanodine receptor mRNA levels among the three groups. SR Ca2+-ATPase gene expression was downregulated in human atrial tissue with TR but not in ASD, which might have resulted from the differences in the degree and/or the type of hemodynamic overload to the myocardium.
authors.affiliation: Research Institute of Angiocardiology, Cardiovascular Clinic, Faculty of Medicine, Kyushu University School of Medicine, Fukuoka, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Sadamatsu
authors.forename: Y
authors.initials: Y
authors.lastname: Urabe
authors.forename: H
authors.initials: H
authors.lastname: Tsutsui
authors.forename: H
authors.initials: H
authors.lastname: Tagawa
authors.forename: F
authors.initials: F
authors.lastname: Maruoka
authors.forename: K
authors.initials: K
authors.lastname: Igarashi-Saito
authors.forename: K
authors.initials: K
authors.lastname: Takeda
authors.forename: Y
authors.initials: Y
authors.lastname: Kawachi
authors.forename: H
authors.initials: H
authors.lastname: Yasui
authors.forename: A
authors.initials: A
authors.lastname: Takeshita
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D016280:Atrial Function, Right; D015152:Blotting, Northern; D000252:Calcium-Transporting ATPases / Q000235:genetics* / Q000378:metabolism; D006332:Cardiomegaly / Q000201:enzymology / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D005260:Female; D005355:Fibrosis / Q000378:metabolism / Q000473:pathology; D015870:Gene Expression; D006325:Heart Atria / Q000201:enzymology* / Q000503:physiopathology / Q000648:ultrastructure; D006344:Heart Septal Defects, Atrial / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000201:enzymology* / Q000648:ultrastructure; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism*; D012519:Sarcoplasmic Reticulum / Q000201:enzymology* / Q000648:ultrastructure; D014262:Tricuspid Valve Insufficiency / Q000150:complications / Q000473:pathology / Q000503:physiopathology
chemical_list: D012333:RNA, Messenger; D000252:Calcium-Transporting ATPases