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Heat shock protects endotheliocyte actin cytoskeleton from destruction under conditions of ATP depletion: Role of heat shock protein HSP27

  • Morphology and Pathomorphology
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Bulletin of Experimental Biology and Medicine Aims and scope

Abstract

Heat shock followed by 12–18-hour recovery induced tolerance of cultured endothelial cells to ATP depletion preventing degradation of actin filaments and HSP27 dephosphorylation/redistribution. HSP27 accumulates during this period, while inhibition of protein synthesis abolishes the protective effect of heat shock.

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Authors and Affiliations

  1. Russian Cardiology Research and Production Complex, Institute of Experimental Cardiology, Ministry of Health, Moscow

    S. A. Loktionova, O. P. Il'inskaya, E. M. Tararak & A. L. Bryantsev

  2. Medical Radiology Research Center, Russian Academy of Medical Sciences, Obninsk

    A. E. Kabakov

Authors
  1. S. A. Loktionova
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  2. O. P. Il'inskaya
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  3. E. M. Tararak
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  4. A. L. Bryantsev
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  5. A. E. Kabakov
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Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 127, No. 2, pp. 237–240, February, 1999

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Loktionova, S.A., Il'inskaya, O.P., Tararak, E.M. et al. Heat shock protects endotheliocyte actin cytoskeleton from destruction under conditions of ATP depletion: Role of heat shock protein HSP27. Bull Exp Biol Med 127, 215–218 (1999). https://doi.org/10.1007/BF02433120

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  • DOI: https://doi.org/10.1007/BF02433120

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