Age-related regeneration decline conundrum

Over a 16-year period, Panagiotis Tsonis at the University of Dayton, Ohio, and colleagues removed the lenses of six Japanese newts (Cynops pyrrhogaster) 18 times. After each excision, the lenses regenerated. They did so not from remaining lens tissue, but from pigment epithelial cells in the upper part of the iris. There was no documented decline in regenerative capacity neihter due to aging, nor to repetition.

The paper published in Nature Communications reports: “In addition, despite beliefs that aged animals regenerate less efficiently than young ones (also discussed by Darwin), our experiments show that this is not the case in the newt. As regenerative medicine has entered a new era, the knowledge that aged tissues possess robust regenerative capabilities should provide the impetus to identify mechanisms underlying this capacity in the newt and compare them with strategies being employed to promote mammalian regeneration, such as the creation of iPS cells.”

Unfortunately, the authors don’t discuss possible mechanisms underlying such an extraordinary capacity. This absolutely has to be studied, because these mechanisms, when identified, may shed light at how we can manipulate mammalian and human cells in order to trigger at least somewhat similar effects. I find restoration of own regenerative capacity to be a very potent way of extending our lives, therefore this work in newts and other animals with fantastic regenerative abilities has to be continued and multiplied. Any ideas about how this may be done are welcome.



Filed under Article, Tissue rejuvenation

5 responses to “Age-related regeneration decline conundrum

  1. I think the best bet is to reprogram one’s DNA so that either suppressed such abilities are triggered or they are transplanted from the newt genome. It would have to be a personalized treatment, obviously, and initially it would be extremely costly, but I tend to think this is possible, why molecular biologists are not keen on it, I don’t know, they probably consider this to be very risky as changing the DNA of every cell cannot be done error-prone, therefore it would need a kind of error recovery, it is extremely non-trivial do not take me wrong 🙂

  2. Pingback: Age-related regeneration decline conundrum (via Maria Konovalenko) | Business, Technology and the Future

  3. Brett Mack

    Perhaps a torrent of telomerase activity causes the rapid division / regeneration of the cells? I suppose in the newt, it would be highly controlled if they aren’t getting cancer from it!

  4. Mitchell Porter

    A very quick look at the literature has introduced me to a whole new way to think about tissue and organ regeneration: You want some of the remaining cells in the tissue to dedifferentiate into progenitor cells, which are like tissue-specific stem cells, which (if all goes well) will then replicate a limited number of times and differentiate approriately, restoring the tissue. In this article, deletion of the p21 gene turns a “nonhealer” mouse into one that is “regeneration-competent”. So maybe, if you were regrowing an organ in an organism that is not naturally a regenerator, like a human being, you could use silencing RNA to suppress p21 at the regeneration site.

  5. Indeed, the MRL mouse strain is extraordinary in the way how they are able to completely heal damage from a myocardial infarction, for example. That’s exactly what I’m talking about – we have to have more experiments like these, studing the intrinsic mechanisms of regeneration, so we could kknow for sure if it’s the telomerase activity, p21 supression or a combination of other things.

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