Peptide Promotes Overcoming of the Division Limit in Human Somatic Cell

  • V. Kh. Khavinson
  • I. E. Bondarev
  • A. A. Butyugov
  • T. D. Smirnova


We previously showed that treatment of normal human diploid cells with Epithalon (Ala-Glu-Asp-Gly) induced expression of telomerase catalytic subunit, its enzymatic activity, and elongation of telomeres. Here we studied the effect of this peptide on proliferative potential of human fetal fibroblasts. Primary pulmonary fibroblasts derived from a 24-week fetus lost the proliferative potential at the 34th passage. The mean size of telomeres in these cells was appreciably lower than during early passages (passage 10). Addition of Epithalon to aging cells in culture induced elongation of telomeres to the size comparable to their length during early passages. Peptide-treated cells with elongated telomeres made 10 extra divisions (44 passages) in comparison with the control and continued dividing. Hence, Epithalon prolonged the vital cycle of normal human cells due to overcoming the Heyflick limit.

peptide Epithalon telomeres fibroblasts aging 


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  1. 1.
    S. V. Anisimov, K. P. Bokheler, V. Kh. Khavinson, and V. N. Anisimov, Byull. Eksp. Biol. Med., 133, No. 3, 340–347 (2002).Google Scholar
  2. 2.
    S. V. Rozenfel'd, E. F. Togo, V. S. Mikheev, et al., Ibid., 320–322.Google Scholar
  3. 3.
    V.Kh.Khavinson, I.E. Bondarevand, and A.A. Butyugov Ibid. 135, No. 6, 692–695 (2003).Google Scholar
  4. 4.
    V.Kh. Khavinson, I.E.Bondarevand, A.A. Butyugov Ibid. 134 No. 10 451–455 (2002).Google Scholar
  5. 5.
    V. N. Anisimov, V. K. Khavinson, A. I. Mikhalski, and A. I. Yashin, Mech. Aging Dev., 122, No. 1, 41–68 (2001).Google Scholar
  6. 6.
    V. N. Anisimov, V. K. Khavinson, I. G. Popovich, and M. A. Zabezhinski, Cancer Lett., 183, 1–8 (2002).Google Scholar
  7. 7.
    V. N. Anisimov, V. Kh. Khavinson, M. Provinciali, et al., Int. J. Cancer, 101. No. 1, 7–10 (2002).Google Scholar
  8. 8.
    L. W. Elmore and S. E. Holt, Mol. Carcinog., 28, No. 1, 1–4 (2000).Google Scholar
  9. 9.
    L. Heyflick, Exp. Gerontol., 38, Nos. 11-12, 1231–1241 (2003).Google Scholar
  10. 10.
    V. Kh. Khavinson, Neuroendocrinol. Lett., 23, Suppl. 3, 11–144 (2002).Google Scholar
  11. 11.
    V. Kh. Khavinson, N. Goncharova, and B. Lapin, Ibid., 22, No. 4, 251–254 (2001).Google Scholar
  12. 12.
    M. Meyerson, C. Counter, E. N. Eaton, et al., Cell, 90, No. 4, 785–795 (1997).Google Scholar
  13. 13.
    N. Rufer, W. Dragowska, G. Thornbury, et al., Nat. Biotechnol., 16, No. 8, 743–747 (1998).Google Scholar
  14. 14.
    W. E. Wright and J. W. Shay, Ibid., 20, No. 7, 682–688 (2002).Google Scholar

Copyright information

© Plenum Publishing Corporation 2004

Authors and Affiliations

  • V. Kh. Khavinson
    • 1
  • I. E. Bondarev
    • 1
  • A. A. Butyugov
    • 1
  • T. D. Smirnova
    • 1
  1. 1.St. Petersburg Institute of Bioregulation and gerontologyNorth-Western Division of Russian Academy of Medical SciencesRussia

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