Cells and Aging

James james at ryley.com
Mon Mar 8 13:47:34 EST 1999

Thomas Mahoney wrote:
> In article <36E2C578.49500488 at ryley.com>, james at ryley.com says...
> >
> >Thomas Mahoney wrote:
> >
> >[snip]
> >
> >> This would help explain why insulin-like growth factor, (IGF), could
> induce
> >> satellite cells to produce new muscle cells in the elderly but only to a
> >> limited degree.  The IGF stimulates the satellite cells and allows them to
> >> produce new muscle cells but their capacity may be limited by their
> shortened
> >> telomeres.
> >
> >This explanation doesn't work well with the fact that people with
> >a variety of muscular dystrophies experience cell
> >degeneration/regeneration for nearly their entire lives, and
> >don't run out of replicative capacity.  For instance, people with
> >FSHD have a normal life expectancy, but must go through MANY MANY
> >more divisions of their satellite cells than normal individuals.
> >Ergo, according to your reasoning, if it was caused by telomere
> >loss in satellite cells, healthy individuals should have a huge
> >reserve potential even in old age.
> >
> >Sincerely,
> >James
> If you have some research cites that show that the replicative capacity of
> satellite cells is not diminished in some muscular dystrophies I would very
> much like to review them.
> The research I have been able to find indicates the exact opposite.  See;
> 1) Wright WE, Exp Cell Res 1985 Apr;157(2):343-54 "Myoblast senescence in
> muscular dystrophy."
> 2) Ontell MP, et al, J Neurobiol 1992 Jun;23(4):407-19 "Transient neonatal
> denervation alters the proliferative capacity of myosatellite cells in
> dystrophic (129ReJdy/dy) muscle."
> 3) Schultz E, Lipton BH, Mech Ageing Dev 1982 Dec;20(4):377-83 "Skeletal
> muscle satellite cells: changes in proliferation potential as a function of
> age."
> Thomas Mahoney, Pres.
> Lifeline Laboratories, Inc.
> http://home.earthlink.net/~excelife/index.html

I didn't say it wasn't diminished.  I said it was sufficient for
them to lead normal lives in many cases.  The point is this:  If
a person with muscular dystrophy can go through 4X (just to pick
a number -- there is no basis for that number, but whether it is
really 2X or 20X the argument still holds) as many satellite cell
divisions throughout the course of their life, and still have
some reserve potential left during old age, that means that a
person without muscular dystrophy should have 4 times more
replicative potential than they need.  So, how can you argue that
a normal old person is anywhere near having a problem with
replicative potential of their satellite cells?

James Ryley

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