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Desialylation Decreases the Resistance of Apo B-Containing Lipoproteins to Aggregation and Increases Their Atherogenic Potential

  • A. A. Mel'nichenkoEmail author
  • V. V. Tertov
  • O. A. Ivanova
  • D. V. Aksenov
  • I. A. Sobenin
  • E. V. Popov
  • V. V. Kaplun
  • I. V. Suprun
  • O. M. Panasenko
  • A. N. Orekhov
Article

Abstract

Subfractions of apo B-containing lipoproteins (VLDL and intermediate-density lipoproteins) with reduced content of sialic acid were found in human blood. These lipoproteins are characterized by high capacity to spontaneous association (aggregation) and stimulated accumulation of cholesterol in smooth muscle cells of human aortic intima. In vitro treatment of apo B-containing lipoproteins with α-2,6-sialidase and α-2,3-sialidase stimulated aggregation and increased the ability of these particles to potentiate cholesterol accumulation in smooth muscle cells of the intact human aortic intima. Probably, desialylation of various apo B-containing lipoproteins can occur in the blood; this process decreases their resistance to aggregation, and increases the ability of these particles to stimulate accumulation of cholesterol in human aortic intima cells, i.e. increases their atherogenic potential.

Key Words

sialic acid sialidase desialylated lipoproteins aggregation of lipoproteins atherosclerosis 

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REFERENCES

  1. 1.
    I. Filipovic, G. Schwarzmann, W. Mraz, et al., Eur. J. Biochem., 93, 51–55 (1979).CrossRefPubMedGoogle Scholar
  2. 2.
    A. Hara and N. S. Radin, Anal. Biochem., 90, 420–426 (1978).CrossRefPubMedGoogle Scholar
  3. 3.
    M. La Belle and R. M. Krauss, J. Lipid Res., 31, 1577–1588 (1990).PubMedGoogle Scholar
  4. 4.
    A. N. Orekhov, V. V. Tertov, and D. N. Mukhin, Atherosclerosis, 86, 153–161 (1991).CrossRefPubMedGoogle Scholar
  5. 5.
    A. N. Orekhov, V. V. Tertov, D. N. Mukhin, and I. A. Mikhailenko, Biochem. Biophys. Res. Commun., 162, 206–211 (1989).CrossRefPubMedGoogle Scholar
  6. 6.
    A. N. Orekhov, V. V. Tertov, I. A. Sobenin, et al., J. Lipid Res., 33, 805–807 (1992).PubMedGoogle Scholar
  7. 7.
    P. Roggentin, R. Schauer, L. L. Hoyer, and E. R. Vimr, Mol. Microbiol., 9, 915–921 (1993).PubMedGoogle Scholar
  8. 8.
    I. A. Sobenin, V. V. Tertov, and A. N. Orekhov, J. Lipid Res., 39, 2293–2299 (1998).PubMedGoogle Scholar
  9. 9.
    V. V. Tertov, V. V. Kaplun, I. A. Sobenin, and A. N. Orekhov, Ibid., 138, 183–195 (1998).Google Scholar
  10. 10.
    V. V. Tertov, A. N. Orekhov, I. A. Sobenin, et al., Circ. Res., 71, 218–228 (1992).PubMedGoogle Scholar
  11. 11.
    V. V. Tertov, A. N. Orekhov, I. A. Sobenin, et al., J. Lipid Res., 34, 365–375 (1993).PubMedGoogle Scholar
  12. 12.
    V. V. Tertov, I. A. Sobenin, Z. A. Gabbasov, et al., Lab. Invest., 67, 665–675 (1992).PubMedGoogle Scholar

Copyright information

© Springer Science+Business Media, Inc. 2005

Authors and Affiliations

  • A. A. Mel'nichenko
    • 1
    Email author
  • V. V. Tertov
    • 2
  • O. A. Ivanova
    • 1
  • D. V. Aksenov
    • 3
  • I. A. Sobenin
    • 2
    • 3
  • E. V. Popov
    • 2
  • V. V. Kaplun
    • 2
  • I. V. Suprun
    • 2
  • O. M. Panasenko
    • 1
    • 2
  • A. N. Orekhov
    • 3
    • 4
  1. 1.Laboratory of Physicochemical Methods for Study and Analysis, Institute of Physicochemical MedicineRussian Ministry of HealthMoscowRussia
  2. 2.Laboratory of Mechanisms for Atherogenesis, Institute of Experimental Cardiology, Russian Research and Production Complex of CardiologyRussian Ministry of HealthMoscowRussia
  3. 3.Laboratory of Intercellular Interactions, Institute of General Pathology and PathophysiologyRussian Academy of Medical SciencesMoscowRussia
  4. 4.Institute of AtherosclerosisRussian Academy of Natural SciencesMoscowRussia

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