In article <6pvtc9$m34$1 at holly.prod.itd.earthlink.net>,
excelife at earthlink.net (Excelife) wrote:
>As Dr. Ames pointed out trauma to epidermal cells will cause the remaining
Assuming you refer to myself rather than my namesake at the University
of California, I must inform that I am but a humble "Mister".
>Following Toms' reasoning, the inability to grow skin cells in vitro earlier
>wasn't that they had hit their "Hayflick Limit" but rather because it took to
>long for them to replicate. The growth factors are able to overcome this
>limitation as mentioned above. However, since they may not be having any
>effect on the telomeres then their potential replicative capacity may be
>shortened.
You might want to review the effect of Interleukin-6 on telomeres.
IL-6 is largely homologous with LIF and CNTF [1] and, like LIF, is
pleiotropic. For the most part it is harmful to our health, but it
also upregulates telomerase in human hematopoietic progenitor cells.
This reduces the shortening of telomere length in the new cells [2,3].
1. Husmann I, Soulet L, et al. 1996. Growth factors in skeletal
muscle regeneration. Cytokine Growth Factor Rev. 7(3):249-258.
2. Santiago-Schwarz, F., J. Tucci, and S.E. Carsons.
Endogenously produced interleukin 6 is an accessory cytokine for
dendritic cell hematopoiesis. Stem.Cells 14:225-231, 1996.
3. Engelhardt, M., R. Kumar, J. Albanell, R. Pettengell, W. Han, and
M.A. Moore. Telomerase regulation, cell cycle, and telomere
stability in primitive hematopoietic cells. Blood 90:182-193,
1997.
