The Change of Expression of Troponin T and I Isoforms in the Failing Myocardium of Rat after Myocardial Infarction.
10.4070/kcj.1996.26.4.872
- Author:
Young Dae KIM
;
In Hoo KIM
;
Jong Seong KIM
;
Hyo Soo KIM
;
Sang Hyun KIM
;
Dae Won SOHN
;
Cheol Ho KIM
;
Byung Hee OH
;
Myoung Mook LEE
;
Young Bae PARK
;
Yun Shik CHOI
;
Jung Don SEO
;
Young Woo LEE
;
James D POTTER
- Publication Type:Original Article
- Keywords:
Postinfarction heart failure;
Rat myocardium;
Troponin T & I isoforms
- MeSH:
Adult;
Animals;
Blotting, Western;
Coronary Vessels;
DNA, Complementary;
Fetal Heart;
Heart;
Heart Failure;
Humans;
Immunoblotting;
Ligation;
Myocardial Infarction*;
Myocardium*;
Myofibrils;
Protein Isoforms*;
Rats*;
Rats, Sprague-Dawley;
Troponin I;
Troponin T*;
Troponin*
- From:Korean Circulation Journal
1996;26(4):872-886
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Contractile dysfunction of rat myocardium in postinfarction remodeling is characterized by decreased response of myofilament both to calcium(Ca++) and adrenergic stimuli. This study tested the hypothesis that above alterations may be linked to molecular switches among the isoforms of troponin T and troponin I, the major regulators of myocardial responsiveness. METHODS: Using Sprague-Dawley rat as a model, myocardiums of fetal heart, 1 day postnatal heart, normal adult heart(n=4), and non-infarcted area of postinfarction heart(n=4, 3 months after left coronary artery ligation, mean LVEDP=21.4mmHg) were studied. For the detection on molecular switches, western blotting and semiquantitative RT-PCR were employed. RESULTS: Immunoblotting of rat myocardium showed normal developmental isoform switch of troponin protein. There was distinct isoform patterns specific for postinfarction rat heart. The postinfarction myocardium developed a marked increase in the fetal isoform and marked decrease in the adult isoform of troponin T, resulting in the reversed ratio of fetal/adult cardiac troponin T isoform(normal adult rat=0.60+/-0.1 vs postinfarction rat=1.79+/-0.15, p<0.01). Also, the postinfarction heart showed approximately 20% decrease in the amount of adult troponin I isoform. In RT-PCR experiments, the postinfarction hearts were characterized by increased amplification of fetal troponin R isoform cDNA(fetal troponin R/GAPDH ; normal adult rat=0.22, postinfarction rat=0.84). However, there was no siginificant difference in the amplification of troponin I cDNA between normal and postinfarction heart. CONCLUSION: These experimental findings indicate that there are molecular switches operative among the regulatory protein troponin T and I in the rat myocardium with development of postianfarction heart failure.
