350 rub
Journal №5 for 2012 г.
Article in number:
Biochemical investigation of left ventricular myocardial cell apoptosis in experimental arterial hypertension
Authors:
M.M. Azova, M.L. Blagonravov, V.A. Frolov
Abstract:
Arterial hypertension (AH) is one of the dominant cardiovascular disorders that can often result in heart failure. It has been suggested that apoptosis may play a key role in heart failure as it causes the progressive loss of cardiomyocytes. Despite of many experimental data in this area, regulators of death and survival pathways in myocardial cell response to AH require further study. The experiment was performed on adult male Chinchilla rabbits in which arterial hypertension was modeled by abdominal aorta banding by 1/3 of its initial diameter. 1, 2 and 4 weeks later caspase-3 activity was measured in left ventricular myocardial cells. The activity significantly increased 4 weeks after modeling of AH. These results demonstrated enhanced apoptosis in left ventricular myocardial cells in experimental arterial hypertension. Caspase-8 activity was determined at 4 weeks after surgery. Absence of significant increasing of the activity indicated the predominance of intrinsic apoptogenic signals.
Pages: 27-31
References
  1. Фролов В.А., Дроздова Г.А., Мустяца В.Ф., Благонравов М.Л. Гипотензивная терапия и сердце: Монография. М.: РУДН. 2009. 292 с.
  2. Бершова Т.В., Монаенкова С.В., Гасанов А.Г. Патогенетическое значение апоптоза кардиомиоцитов при сердечной недостаточности // Педиатрия. 2009. Т. 88. № 1. С. 147-154.
  3. Li Z., Bing O.H., Long X., Robinson K.G., Lakatta E.G. Increased cardiomyocyte apoptosis during the transition to heart failure in the spontaneously hypertensive rat // Am. J. Physiol. 1997. № 272 (5 Pt 2). Р. H2313-2319.
  4. Petrovic D. Cytopathological basis of heart failure--cardiomyocyte apoptosis, interstitial fibrosis and inflammatory cell response // Folia Biol (Praha). 2004. V. 50. № 2. P. 58-62.
  5. Манских В.Н. Морфологические методы верификации и количественной оценки апоптоза // Бюллетень сибирской медицины. 2004. № 1. С. 63-70.
  6. Takemura G., Fujiwara H. Morphological aspects of apoptosis in heart diseases // J. Cell. Mol. Med. 2006. V. 10. № 1. P. 56-75.
  7. Hengartner M.O. The biochemistry of apoptosis // Nature. 2000. № 407. P. 770-776.
  8. Robertson J.D., Zhivotovsky B. New Methodology is a Key to Progress // Cell Cycle. 2002. V. 1 №2. P. 119-121.
  9. Благонравов М.Л., Азова М.М., Фролов В.А. Биохимическое исследование апоптоза клеток миокарда при острой перегрузке левого желудочка в эксперименте // Вопросы биологической, медицинской и фармацевтической химии. 2010. № 8. С. 49-53.
  10. Gonzalez A., Fortuno M.A., Ravassa S. et al. Cardiomyocyte apoptosis in hypertensive cardiomyopathy // Cardiovasc. Res. 2003. № 59. Р. 549-562.
  11. Cheng W., Li B., Kajstura J. et al. Stretch-induced programmed myocyte cell death // J. Clin. Invest. 1995. № 96. Р. 2247-2259.
  12. Fortuño M.A., González A., Ravassa S. et al. Clinical implications of apoptosis in hypertensive heart disease // Am. J. Physiol. Heart Circ. Physiol. 2003. V. 284. № 5. Р. H1495-506.
  13. Leri A., Claudio P.P., Li Q. et al. Stretch-mediated release of angiotensin II induces myocyte apoptosis by activating p53
    that enhances the local rennin-angiotensin system and decreases the Bcl-2-to-Bax protein ratio in the cell // J. Clin. Invest. 1998. № 101. Р. 1326-1342.
  14. De Angelis N., Fiordaliso F., Latini R. et al. Appraisal of the role of angiotensin II and aldosterone in ventricular myocyte apoptosis in adult normotensive rat // J. Mol. Cell Cardiol. 2002. V. 34. №12. Р. 1655-1665.
  15. Lemasters J.J., Theruvath T.P., Zhong Z., Nieminen A.L. Mitochondrial calcium and the permeability transition in cell death // Biochim. Biophys. Acta. 2009. V. 1787. № 11. Р. 1395-1401.
  16. Chen X., Zhang X., Kubo H. et al. Ca2+ influx-induced sarcoplasmic reticulum Ca2+ overload causes mitochondrial-dependent apoptosis in ventricular myocytes // Circ. Res. 2005. V. 97. № 10. P. 1009-1017.
  17. Постнов Ю.В. О роли недостаточности митохондриального энергообразования в развитии первичной гипертензии: нейрогенная составляющая патогенеза гипертензии // Кардиология. 2004. № 6. С. 52-58.
  18. Li G.Y., Fan B., Su G.F.Acute energy reduction induces caspase-dependent apoptosis and activates p53 in retinal ganglion cells (RGC-5) // Exp. Eye Res.2009. V. 89. № 4. P. 581-589
  19. Samali A., O-Mahoney M., Reeve J. et al.Identification of an inhibitor of caspase activation from heart extracts; ATP blocks apoptosome formation // Apoptosis. 2007. V. 12. № 3.P. 465-474.