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Epigenetic clock analyses of cellular senescence and ageing

telomeres epigenetic senescence aging

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#1 corb

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Posted 19 February 2016 - 04:03 PM


 

A confounding aspect of biological ageing is the nature and role of senescent cells. It is unclear whether the three major types of cellular senescence, namely replicative senescence, oncogene-induced senescence and DNA damage-induced senescence are descriptions of the same phenomenon instigated by different sources, or if each of these is distinct, and how they are associated with ageing. Recently, we devised an epigenetic clock with unprecedented accuracy and precision based on very specific DNA methylation changes that occur in function of age. Using primary cells, telomerase-expressing cells and oncogene-expressing cells of the same genetic background, we show that induction of replicative senescence (RS) and oncogene-induced senescence (OIS) are accompanied by ageing of the cell. However, senescence induced by DNA damage is not, even though RS and OIS activate the cellular DNA damage response pathway, highlighting the independence of senescence from cellular ageing. Consistent with this, we observed that telomerase-immortalised cells aged in culture without having been treated with any senescence inducers or DNA-damaging agents, re-affirming the independence of the process of ageing from telomeres and senescence. Collectively, our results reveal that cellular ageing is distinct from cellular senescence and independent of DNA damage response and telomere length.

 

http://www.impactjou...83&path[]=21162


Edited by corb, 19 February 2016 - 04:04 PM.


#2 niner

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Posted 19 February 2016 - 09:52 PM

This result may be disturbing to those who see telomerase as "the answer".



#3 corb

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Posted 19 February 2016 - 10:54 PM

Even Josh Mitteldorf says the cause is multifactorial now (I should rectify - the "cause" to the "clock" is more than one according to him), so I don't think there's that many of them still around. Then again, like Liz Parish, there still might be some who hang on to that idea.

 

 

 

 


Edited by corb, 19 February 2016 - 11:05 PM.


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#4 Logic

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Posted 20 February 2016 - 12:24 AM

Stem and progenitor have high telomerase levels and replace the cells with high cell turnover like those of the gut and immune system.
The gut and immune system in turn shield us from the toxins and pathogens that cause inflammation and the accompanying epigenetic changes that plague long lived cells...

And also from some of the DNA damage caused by virii and other ROS causing pathogens and toxins.

 

The immune system will also take out cells with damaged DNA... if it's still capable...

(There are also means to tweak the DNA repair 'machine'.  Cat's Claw, Selenium and NAD+ upregulators come to mind)

 

So perhaps we are closely examining too many trees to see the woods here?

Note to self: I wonder what effect high cell turnover organs and systems have on Glycation, metal buildup and lipofuscin etc..?


Edited by Logic, 20 February 2016 - 12:26 AM.

  • unsure x 1





Also tagged with one or more of these keywords: telomeres, epigenetic, senescence, aging

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