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ISSN 2522-9028 (Print)
ISSN 2522-9036 (Online)
DOI: https://doi.org/10.15407/fz

Fiziologichnyi Zhurnal

is a scientific journal issued by the

Bogomoletz Institute of Physiology
National Academy of Sciences of Ukraine

Editor-in-chief: V.F. Sagach

The journal was founded in 1955 as
1955 – 1977 "Fiziolohichnyi zhurnal" (ISSN 0015 – 3311)
1978 – 1993 "Fiziologicheskii zhurnal" (ISSN 0201 – 8489)
1994 – 2016 "Fiziolohichnyi zhurnal" (ISSN 0201 – 8489)
2017 – "Fiziolohichnyi zhurnal" (ISSN 2522-9028)

Fiziol. Zh. 2005; 51(3): 12-17

Necrotic and autophagic cardiomyocyte cell death in culture

V.E. Dosenko, V.S. Nagibin, L.V. Tumanovskaya,A.A. Moibenko, J.VaagePOSTCONDITIONING PR

    A.A. Bogomoletz Institute of Physiology National Academy ofSciences of Ukraine, Kiev



Abstract

In the paper the data concerning the possibility of the reproduction of the postconditioning phenomena in the cardyomicyte culture are presented. Primary cultures of cardiomyocytes from neonatal rats underwent 30 minutes of anoxia followed by 60 minutes of reoxygenation. Three differ- ent models of postconditioning were used: 3 cycles of 1, 3, or 5 minutes of reoxygenation followed by 1, 3, or 5 minutes of anoxia, respectively. The percentage of living, necrotic, and apoptotic cells were determined by staining with Hoechst 33342 and propidium iodide. Autophagy was demonstrated by the staining of vacuolar structures in vivo by monodansyl cadaverine. After anoxia and reoxygenation the amount of living, necrotic and apoptotic cells were 79±1.5, 7.8±0.9 and 13±1.5 %, respectively (in unstimulated cell culture 90±0.8, 3.3±0.3, and 5.5±0.7, P<0.0001 for all). Postconditioning with 1 min anoxia 3-fold increased the amount of living cells and decreased the number of necrotic and apoptotic cells (P=0.002, P=0.02 and P=0.043 respectively). Postconditioning with cycles of 3 and 5 minutes had a gradually reduced effect compared to cycles of 1 minute. The percentage of autophagic cells in control cell culture was 4.3±0.3%. This number increased after anoxia- reoxygenation to 14±0.8%, and was reduced by postconditioning (P<0.001). The data obtained indicate that postconditioning is one of the effective methods of cardioprotection and could ef- fectively decrease the amount of cardiomyocytes with traits of programmed or non-programmed cell death.

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References

  1. Веремеенко К.Н., Досенко В.Е., Нагибин В.С. и др.Протеолитические ферменты и апоптоз // Укр.биохим. журнал. – 2003. – №4. – С.20–34.
  2. Мойбенко О.О., Юзьків М.Я., Тумановська Л.В.,Kоцюруба А.В. Гостра ішемія-реперфузія міокар-да: роль NO системи // Фізіол. журн. – 2004. – 50,№2. – P.34–41.
  3. Нагібін В.С., Досенко В.Є., Пивовар С.М. и др.Фторований аналог діазоксиду попереджує апоптознеонатальних кардіоміоцитів під час аноксії–реоксигенації // Там само. –2004. – 50, № 3. – С.3–9.
  4. Тумановська Л.В., Досенко В.Є., Нагібін В.С. и др.Апоптотична, аутофагічна та онкотична загибелькардіоміоцитів при аноксії-реоксигенації // Там само. –2004. – 50, №5. –P.11–19.
  5. Aki T., Yamaguchi K., Fujimiya T., Mizukami Y.Phosphoinositide 3-kinase accelerates autophagic celldeath during glucose deprivation in the rat cardio-myocyte-derived line H9c2 // Oncogene. – 2003. – 22,№52. – P.8529–8535.
  6. Bulteau A.-L., Lundberg K.C., Humphries K.M. et al.Oxidative modification and inactivation of theproteasome during coronary occlusion/reperfusion //J. Biol. Chem. – 2001. – 276, № 32. – P.30057–30063.
  7. Bursch W. The autophagosomal-lysosomal compart-ment in programmed cell death // Cell Death Differ. –2001. – 8. – P.569–581.
  8. Galagudza M., Kurapeev D., Minasian S. et al. Is-chemic postconditioning: brief ischemia duringreperfusion converts persistent ventricular fibrillationinto regular rhythm // Eur. J. Cardiothorac. Surg. – 2004. –25, №6. – P.1006–1010.
  9. 9. Kin H., Zhao Z.Q., Sun H.Y. et al. Postconditioningattenuates myocardial ischemia-reperfusion injury byinhibiting events in the early minutes of reperfusion //Cardiovasc. Res. –2004. –62, №1. – P.74–85.
  10. 10. Klionsky D.J., Emr S.D. Autophagy as a regulatedpathway of cellular degradation // Science. – 2000. –290. – P.1717–1721.
  11. Kostin S., Pool L., Elsasser A. et al. Myocytes die bymultiple mechanisms in failing human heart // Circulat.Res. – 2003. – 92, №7. – P.715–724.
  12. Munafo D.B., Colombo M.I. A novel assay to studyautophagy: regulation of autophagosome vacuole sizeby amino acid deprivation // J. Cell Science. – 2001. –114. – P.3619–3629
  13. Reinecke H., Zhang M., Bartosek T., Charles E.M. Sur-vival, integration, and differentiation of cardiomyocytegrafts // Circulation. –1999. – 100. –№2. – P.193–202.
  14. Reusner C., Werschy S., Sutterlin S. et al. Postconditioningof the rat heart by I/R reduces the infarct size in vivo butnot in vitro and does not involve p38 MAPK or PKC // J.Mol. Cell. Cardiol. – 2004. –36, Issue 5. – P.753.
  15. Shimomura H., Terasaki F., Hayashi T. et al. Autoph-agic degeneration as a possible mechanism of myocar-dial cell death in dilated cardiomyopathy // Jаp.Circulat. J. – 2001. – 65. –P.965–968.
  16. Sperandio S., De Belle I., Bredesen D. An alternative,nonapoptotic form of programmed cell death // Proc.Natl. Acad. Sci. USA. – 2000. – 97, №26. – P.14376–14381.
  17. Terman A., Dalen H., Eaton J.W. et al. Mitochondrialrecycling and aging of cardiac myocytes: the role ofautophagocytosis // Exp. Gerontol. – 2003. –38, №8. –P.863–876.
  18. Tsang A., Hausenloy D.J., Mocanu M.M., Yellon D.M.Postconditioning: a form of «modified reperfusion»protects the myocardium by activating the phospha-tidylinositol 3-kinase-Akt pathway // Circulat. Res. –2004. – 95, №3. – P.230–232.
  19. 19. Yang X.M., Proctor J.B., Cui L. et al. Multiple, briefcoronary occlusions during early reperfusion protectrabbit hearts by targeting cell signaling pathways // J.Amer. Coll. Cardiol. –2004. – 44, №5. – P.1103–1110.
  20. 20. Zhao Z.Q., Corvera J.S., Halkos M.E. et al. Inhibitionof myocardial injury by ischemic postconditioningduring reperfusion: comparison with ischemic precondi-tioning // Amer. J. Physiol. – Heart Circulat. Physiol. –2003. –285, №2. – H.579–588.
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