title: Differences in expression of sarcoplasmic reticulum Ca2+-ATPase and Na+-Ca2+ exchanger genes between adjacent and remote noninfarcted myocardium after myocardial infarction.
abstract: Although cardiac failure can develop over time after myocardial infarction, the mechanism responsible for this is still unknown. The change of intracellular Ca2+ transport protein, such as sarcoplasmic reticulum (SR) Ca2+-ATPase (SR-Ca2+), Na+-Ca2+ exchanger (Na+-Ca2+), or cardiac phenotypic modulation of contractile protein in noninfarcted myocardium may have a important role. However, the time course in gene expression of sarcoplasmic reticulum (SR) Ca2+-ATPase (SR-Ca2+), Na+-Ca2+ exchanger (Na+-Ca2+), and contractile protein in the adjacent and remote noninfarcted myocardium after myocardial infarction has not been examined. At 1, 3 weeks and 3 months after myocardial infarction, hemodynamics were measured and mRNA of the left ventricle was analyzed. Left ventricular end-diastolic volume and weight increased both with time. Ascites became apparent at 3 months after infarction. SR-Ca2+ mRNA levels in the adjacent noninfarcted myocardium were 0.7- (P<0.01), 0.9- (N.S.), and 0.7-fold (P<0.01) of control, and Na+-Ca2+ mRNA levels were 2.1- (P<0.01), 1.4- (P<0.01), and 0.8-fold (P<0.01) of control, at 1, 3 weeks and 3 months after infarction, respectively. beta-Myosin heavy chain (MHC) mRNA was increased to 2.1- (P<0.01), 1.5- (P<0.01), and 1.4-fold (P<0.01), and alpha-skeletal actin was increased to 2.4- (P<0.01), 3.8- (P<0.01), and 1.6-fold (P<0.01) control levels, at 1 week, 3 weeks and 3 months, respectively. In contrast, alpha-MHC mRNA level was decreased at 1 week and 3 months after infarction. alpha-cardiac actin mRNA level did not change over time after infarction. In the remote non-infarcted myocardium, beta-MHC, alpha-skeletal actin, and Na+-Ca2+ mRNA levels were increased, but SR-Ca2+, alpha-MHC, and alpha-cardiac actin mRNA did not change after infarction. These findings suggest that: (1) intracellular Ca2+ handling system after myocardial infarction may be different between adjacent and remote non-infarcted myocardium: and that (2) both decreased gene expression of SR Ca2+-ATPase and Na+-Ca2+ exchanger in the adjacent non-infarcted myocardium may progress cardiac dysfunction.
authors.affiliation: First Department of Internal Medicine, Osaka City University Medical School, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Yoshiyama
authors.forename: K
authors.initials: K
authors.lastname: Takeuchi
authors.forename: A
authors.initials: A
authors.lastname: Hanatani
authors.forename: S
authors.initials: S
authors.lastname: Kim
authors.forename: T
authors.initials: T
authors.lastname: Omura
authors.forename: I
authors.initials: I
authors.lastname: Toda
authors.forename: M
authors.initials: M
authors.lastname: Teragaki
authors.forename: K
authors.initials: K
authors.lastname: Akioka
authors.forename: H
authors.initials: H
authors.lastname: Iwao
authors.forename: J
authors.initials: J
authors.lastname: Yoshikawa
mesh_terms: D000818:Animals; D001202:Ascitic Fluid / Q000378:metabolism; D009320:Atrial Natriuretic Factor / Q000235:genetics; D002118:Calcium / Q000378:metabolism*; D002352:Carrier Proteins / Q000235:genetics*; D003285:Contractile Proteins / Q000235:genetics; D005786:Gene Expression Regulation / Q000502:physiology*; D015971:Gene Expression Regulation, Enzymologic / Q000502:physiology*; D006352:Heart Ventricles / Q000378:metabolism; D006439:Hemodynamics / Q000502:physiology; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012519:Sarcoplasmic Reticulum / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism*; D019831:Sodium-Calcium Exchanger; D016276:Ventricular Function
chemical_list: D002352:Carrier Proteins; D003285:Contractile Proteins; D019831:Sodium-Calcium Exchanger; D009320:Atrial Natriuretic Factor; D012964:Sodium; D002118:Calcium