Re-Visiting a Post by Lou Pagnucco
james at nospam.com
Sun Oct 25 11:12:47 EST 1998
Lou Pagnucco wrote:
> James <james at nospam.com> wrote in article <3630B0B0.5C76A03E at nospam.com>...
> > > A weaker link in Lou's idea is the question of whether these senescent
> > > fibroblasts are responsible for lax skin etc. It is unclear whether
> > > the overproduction of collagenase would have these effects, since they
> > > are normally ascribed to the disorderly crosslinking of OLD collagen.
> > > Most such collagen should be no less degradable by collagenase than
> > > undamaged collagen, so this overproduction may, if anything, actually
> > > RETARD these features of aging of skin.
> > I would agree with this 100% - if collagenase were the only
> > factor. But I don't think lax skin has much to do with collagen
> > crosslinking (other than some decreased elasticity). I think
> > loss of subcutaneous fat is the culprit here. I don't know why
> > that happens - is it a general hormonal change, or something to
> > do with fibroblasts?
> But don't the cells that adhere to the extracellular matrix
> obtain much of their regulatory signals from the ECM?
> Isn't this a "chicken first or egg first" question?
I guess all cells receive some of their signals that way, but if
we are talking about fat loss then we are talking about
adipocytes, not fibroblasts. I don't really know, but because of
the role they play in the body (and the fact that they don't
divide anyway) it seems more likely to me that adipocytes would
be hormonally regulated rather than regulated largely by the ECM.
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