> Sounds to me like he repeated old experiments with what should be much
> better data, and got different results. That could surely happen, so I am
> leaning towards believing it... But I don't see how cells that are not
> expressing telomerase are maintaining the replicative potential in vivo
> (which is the conclusion I draw from the fact that their replicative
> capacities do not differ significantly when grown in culture), and then
> senescing uniformly in vitro.
>> Were I to follow this line of reasoning to it's logical conclusion the
> answer I arrive at is that the senescence we see in fibroblasts in vitro is
> an artifact of the culture conditions and that they really do not senesce in
> vivo. But that's a little too off the beaten path for me to accept at the
> moment. Maybe it's just late... Anyone else have any thoughts?
I thought that we had already established at some point in these threads
that skin is generated by some kind of basil stem cells which *do*
express telemerase. In which case, in healthy skin the *first*
derivatives of those cells (which replicate outwards to the surface, as
I understand it) would always have new, unshorened telomeres. Only in
those cases where skin is diseased and too quickly needing to be
regenerated, would the basal cells not have time to regenerate their
telomeres before having to replicate again.
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