Here's an article about regenerative fibroblast injections for rejuvenating skin, gums, etc:
http://www.betterhum...ID=2005-05-02-2
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Fibroblast Injections
Started by
manofsan
, May 12 2005 10:29 PM
6 replies to this topic
#2
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Posted 12 May 2005 - 11:17 PM
Isolagen is transplanting the patient's own fibroblasts back after they have been expanded in culture. I wonder, though about how much the Hayflick limit on these cells would affect their lifespan (and consequently the lifespan of the treatment) and if it would not be an improvement to tweak these cells prior to transplantation. Theoretically, if these cells are simply allowed to divide in culture, then they are reaching their Hayflick limit faster than those in the body and could therefore create regions of localised senescence and possibly tumorigenesis. It's a great idea, but potentially disastarous in the long term without modifying these cells to either bring them into the same aging rate as the rest of the body or make them more cancer resistant.
#3
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Posted 14 May 2005 - 04:30 PM
Just to recap -- Hayflick Limit is the telomere-counter limit on the number of cell replications? So that means the more those cells are multiplied, the faster they will run down their counter limit?
Gee, somebody's gotta come up with a solution to that. This is that difference between erosion/oxidation-caused aging, versus pre-programmed innate aging. Sounds like the latter is the cap we need to get rid of first, before we can tackle the former.
Gee, somebody's gotta come up with a solution to that. This is that difference between erosion/oxidation-caused aging, versus pre-programmed innate aging. Sounds like the latter is the cap we need to get rid of first, before we can tackle the former.
#4
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Posted 15 May 2005 - 02:23 AM
A potential solution is transient expression of telomerase in the cultured fibroblasts [1] or the addition of telomerase to the culture medium [sorry I don't have the ref at hand].Gee, somebody's gotta come up with a solution
The wear and tear types of damage might be kept in check by rigorous selection in culture for a while, but in the end we will want to derive replacement cells fresh from the germ line, rather than using the patient's own. Such fresh replacement cells would also have reasonably long telomeres, so I don't see why we should not start using them right away.
#5
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Posted 15 May 2005 - 03:36 AM
addition of telomerase to the culture medium
An interesting solution for the culture/telomere depletion problem (1) provided the telomerase can get inside the cell. Even so, any such treatment would have to be supported by increased genomic stability modulators to offset the extended lifespan of the transiently telomerase positive cells.
(1) J Dermatol Sci. 2004 May;34(3):221-30.
The effect of the long-term cultivation on telomere length and morphology of cultured epidermis.
Miyata Y, Okada K, Fujimoto A, Hata K, Kagami H, Tomita Y, Ueda M.
#6
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Posted 15 May 2005 - 05:22 AM
Well why would you care if some cell culture in a petri dish turns cancerous? Just make sure you have enough cultures to ensure some make it through without cancer, and discard the rest.
Stem cell growth seems so fragile, that it's a wonder we ever make it out of the womb. There must be a whole lot we're missing on the epigenetic side that's going on.
Stem cell growth seems so fragile, that it's a wonder we ever make it out of the womb. There must be a whole lot we're missing on the epigenetic side that's going on.
#7
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Posted 15 May 2005 - 10:16 AM
why would you care if some cell culture in a petri dish turns cancerous?
There are many shades of what we define as cancerous and more importantly pre-cancerous which may not be readily detectable by conventional screening methods (and in any case all you need is one malignant cell) so that following transplantation back into the patient one may have inadvertently increased the likelihood of cancer stemming from the transplanted tissue/cells.
Supposing that in order to prevent the telomere length reduction, due to repeated mitosis in culture, telomerase was introduced into the culture medium as John suggested. This would result in a cell being able to transcend its determined (telomerase-limited) lifespan in terms of cell division but without the other genomic stability (plus other) mechanisms from being similarly upregulated to protect the cell from DNA damage that could lead to cancer (1). Considering that DNA repair enzymes are more abundant and operate differently in stem cells than somatic cells (2, 3) enhancing the proliferative lifespan of fibroblasts without a commensurate increase in genomic stability could well be the path to disaster.
(1) Nucleic Acids Res. 2005 Apr 29;33(8):2475-85.
Repair of cyclobutane pyrimidine dimers or dimethylsulfate damage in DNA is identical in normal or telomerase-immortalized human skin fibroblasts.
Bates SE, Zhou NY, Federico LE, Xia L, O'Connor TR.
(2) Proc Natl Acad Sci U S A. 2002 Aug 6;99(16):10567-70.
Somatic stem cells and the kinetics of mutagenesis and carcinogenesis.
Cairns J.
(3) Annu Rev Med. 2005;56:495-508.
DNA repair defects in stem cell function and aging.
Park Y, Gerson SL.
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