Biopolym. Cell. 2000; 16(5):425-429.
Investigation of molecular mechanism of cardiomyocytes function at dilated cardiomyopathy using the model of mammals myocardium myofibrile reconstruction
1Fedorkova O. M., 1Kovenja T. V., 1Bobyk V. I., 2Ryabenko D. V., 3Tregubov V. S., 3Danilova V. M., 1Sidorik L. L., 1Matsuka G. Kh.
  1. Institute of Molecular Biology and Genetics, NAS of Ukraine
    150, Akademika Zabolotnoho Str., Kyiv, Ukraine, 03680
  2. M. D. Strazhesko Institute of Cardiology, MAS of Ukraine
    5, Narodnogo Opolchennya Str., Kyiv, Ukraine, 03151
  3. Petr Bogach Institute of Physiology
    Taras Shevchenko National University of Kyiv
    2, Academika Glushkova Ave Str., Kyiv, Ukraine, 03187


The method of myocardial myofibril reconstruction from structural (actomyosln) and regulatory (tropomyosin and troponin) proteins has been used. The influence of the regulatory proteins purified from healthy donor's myocardium and from myocardium affected by dilated cardiomyopathy (DCM) on the Mg2+ -ATPase activity of actomyosin from the tissues has been studied by this method. During cross-myofibril reconstruction the sensitivity of desensitive acto-myosin to Ca2+ was restored and it did not depend either on actomyosin or tropomyosin-troponin complex origin. Bovine actomyosin has been used as a standard protein in comparison with human actomyosin during addition of the regulatory proteins. The Mg2+ -ATPase actomyosin activity was 1.5 times lower for DCM patients than for healthy donors. It probably depends on modification changes of contractile proteins during DCM development.


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