Advertisement

Bulletin of Experimental Biology and Medicine

, Volume 140, Issue 4, pp 419–422 | Cite as

Phospholipid Hydrolysis with Phospholipases A2 and C Impairs Apolipoprotein B-100 Conformation on the Surface of Low Density Lipoproteins by Reducing Their Association Resistance

  • D. V. Aksenov
  • A. A. Mel'nichenko
  • I. V. Suprun
  • E. V. Yanushevskaya
  • T. N. Vlasik
  • I. A. Sobenin
  • O. M. PanasenkoEmail author
  • A. N. Orekhov
Article

Abstract

Modification of apolipoprotein B-100 conformation on the surface of LDL isolated from human blood was demonstrated by enzyme immunoassay with a panel of monoclonal antibodies to this protein. The study by the light transmission fluctuation method showed that incubation of LDL with phospholipases A2 or C led to association of LDL particles. This lipolytic modification seems to impair LDL surface properties inducing association of these particles, which can play an important role in lipid accumulation in the vascular wall and at early stages promote the development of atherosclerosis.

Key Words

low density lipoproteins phospholipase A2 phospholipase C lipoprotein aggregation atherosclerosis 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

REFERENCES

  1. 1.
    E. V. Yanushevskaya, N. V. Valentinova, N. V. Medvedeva, et al., Angiol. Sosud. Khir., 5,Suppl., 241–251 (1999).Google Scholar
  2. 2.
    J. K. Hakala, K. Oorni, M. Ala-Korpela, and P. T. Kovanen, Arterioscler. Thromb. Vasc. Biol., 19, 1276–1283 (1999).PubMedGoogle Scholar
  3. 3.
    T. Hevonoja, M. O. Pentikainen, M. T. Hyvonen, et al., Biochim. Biophys. Acta, 1488, 189–210 (2000).PubMedGoogle Scholar
  4. 4.
    E. Hurt-Camejo, G. Camejo, H. Peilot, et al., Circ. Res., 89, 298–304 (2001).PubMedGoogle Scholar
  5. 5.
    K. Oorni, M. O. Pentikainen, M. Ala-Korpela, and P. T. Kovanen, J. Lipid Res., 41, 1703–1715 (2000).PubMedGoogle Scholar
  6. 6.
    A. N. Orekhov, V. V. Tertov, D. N. Mukhin, and I. A. Mikhailenko, Biochem. Biophys. Res. Commun., 162, 206–211 (1989).PubMedCrossRefGoogle Scholar
  7. 7.
    V. V. Tertov, V. V. Kaplun, and A. N. Orekhov, Atherosclerosis, 138, 183–195 (1998).PubMedCrossRefGoogle Scholar
  8. 8.
    V. V. Tertov, I. A. Sobenin, Z. A. Gabbasov, et al., Lab. Invest., 67, 665–675 (1992).PubMedGoogle Scholar
  9. 9.
    V. V. Tertov, I. A. Sobenin, Z. A. Gabbasov, et al., Biochem. Biophys. Res. Commun., 163, 489–494 (1989).PubMedCrossRefGoogle Scholar
  10. 10.
    V. V. Tertov, I. A. Sobenin, Z. A. Gabbasov, et al., Circ. Res., 71, 218–228 (1992).PubMedGoogle Scholar

Copyright information

© Springer Science+Business Media, Inc. 2005

Authors and Affiliations

  • D. V. Aksenov
    • 1
  • A. A. Mel'nichenko
    • 2
  • I. V. Suprun
    • 3
  • E. V. Yanushevskaya
    • 4
  • T. N. Vlasik
    • 4
  • I. A. Sobenin
    • 1
    • 3
  • O. M. Panasenko
    • 2
    • 3
    Email author
  • A. N. Orekhov
    • 1
    • 5
  1. 1.Laboratory of Cell-to-Cell Interactions, Institute of General Pathology and PathophysiologyRussian Academy of Medical SciencesRussia
  2. 2.Laboratory of Physicochemical Methods of Investigation and Analysis, Institute of Physicochemical MedicineMinistry of Health of the Russian FederationRussia
  3. 3.Laboratory of Atherogenesis Mechanisms, Institute of Experimental CardiologyMinistry of Health of the Russian FederationRussia
  4. 4.Laboratory of Cell Engineering, Institute of Experimental CardiologyMinistry of Health of the Russian FederationRussia
  5. 5.Institute of AtherosclerosisRussian Academy of Natural SciencesMoscowRussia

Personalised recommendations