Heart function and cytokine expression is similar in mice and rats after myocardial infarction but differences occur in TNFalpha expression.
Large myocardial infarction (MI) causes substantial cardiac remodeling and often leads to heart failure. The genetically engineered mouse is believed to provide a powerful tool for investigating the underlying pathophysiological mechanisms and for developing new therapeutic strategies. The present study investigates the functional parameters and expression levels of transforming growth factor (TGF) beta isoforms, interleukin-6 (IL-6) and tumor necrosis factor (TNF) alpha, which may be involved in the remodeling mechanisms, in a mouse model of MI; comparisons with data from rats were also made. Female Sprague-Dawley rats ( n=10-12 at each time point) and female Balb/c mice ( n=6-8 at each time point) were used. In both mice and rats MI induced a time-dependent reduction in heart function with subsequent development of heart failure. The hemodynamic consequences after 4 weeks are characterized by reduced left ventricular (LV) developed pressure and increased right ventricular (RV) developed pressure. The pattern of increased expression of most, but not all, of the analyzed cytokines and growth factors is comparable. This emphasizes the important role of these factors in the remodeling processes. However, TNFalpha was more strongly expressed in both the infarct and the non-infarcted area of mice. Since functional and molecular biological parameters can readily be measured in mice with advanced technologies, this qualifies this species as a powerful experimental model, particularly in view of the various transgenic and knock-out mice that are available.
Deten
Alexander
A
Carl-Ludwig-Institute of Physiology, Leipzig University, Liebigstr. 27, 04103 Leipzig, Germany. deta@medizin.uni-leipzig.de
Zimmer
Heinz-Gerd
HG
D000818:Animals; D009320:Atrial Natriuretic Factor / Q000235:genetics; D015415:Biomarkers; D001835:Body Weight; D006332:Cardiomegaly / Q000378:metabolism; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006439:Hemodynamics; D051379:Mice; D008807:Mice, Inbred BALB C; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D020033:Protein Isoforms / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism*; D016277:Ventricular Function, Left
D015415:Biomarkers; D016207:Cytokines; D020033:Protein Isoforms; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D009320:Atrial Natriuretic Factor