LONGECITY

Beauty might only be skin deep, but for those wondering how to keep that skin young, scientists may have found an answer in the form of a protein that encourages cell competition.

The prosaically named COL17A1 might not sound like a fountain of youth, but the new study suggests it does the heavy lifting when it comes to keeping skin intact and unimpaired.

The protein works by encouraging cell competition, a key process to maintain tissue fitness. That effectively "drives out" weaker cells while encouraging replication of stronger ones.

But ageing results in a depletion of COL17A1, as do familiar enemies of youthful skin, like UV radiation.

And when that happens, weaker cells replicate, leaving the skin thinner, more prone to damage and slower to heal.

The research published Thursday in the journal Nature is based on investigations using mice tails, which share many of the same characteristics as human skin.

After confirming the importance of COL17A1, the team decided to investigate whether they could stimulate the protein once it was depleted—effectively looking for compounds that could kickstart the anti-ageing process in skin.

They isolated two chemical compounds—Y27632 and apocynin—and tested both on skin cells, with positive results.

"Application of these drugs to full-thickness skin wounds significantly promoted wound repair," the study said.

The two compounds point to ways of "facilitating skin regeneration and reducing skin ageing," the study added.

In a review of the study commissioned by Nature, two professors from the University of Colorado said cell competition had previously only been studied extensively in fruit flies.

The research "provides evidence that healthy cells in mammals can also efficiently repopulate adults tissues, replacing unfit or damaged cells," wrote professors Ganna Bilousova and James DeGregori.

And they said the research offered "proof-of-principle" that the two chemical compounds could combat ageing.

"Future studies are needed to determine the mechanisms of cell competition in other tissues, and to identify compounds capable of reversing ageing in other organs," they said.

Source: https://medicalxpres...n-youthful.html

What are weaker cells? And how competitive are cancer cells in that regard?

....in mice.

Something to keep an eye on. Seems like it is a rather complicated process. How does the protein trigger "weaker" cells to die or go away?

Very interesting. Apocynin seems to have neuro regenerative properties. 

https://www.ncbi.nlm...pubmed/22202030

and 

https://jneuroinflam...1742-2094-9-241

and it can be extracted from several different plant including licorice. Surprised there is not more research on this. Unfortunately its not available for that average human unless you have a lab. 

This seems to be connected:

Overview
...
Matsumura et al. analyzed hair follicle stem cells during aging. They identified type XVII collagen (COL17A1) as key to hair thinning. DNA damage-induced depletion of COL17A1 triggered cell differentiation resulting in the shedding of epidermal keratinocytes from the skin surface. These changes then caused hair follicle shrinkage and hair loss.

the research article:
Hair follicle aging is driven by transepidermal elimination of stem cells via COL17A1 proteolysis
Matsumura & Mohri & Binh et al. Science 05 Feb 2016

Abstract
Hair thinning and loss are prominent aging phenotypes but have an unknown mechanism. We show that hair follicle stem cell (HFSC) aging causes the stepwise miniaturization of hair follicles and eventual hair loss in wild-type mice and in humans. In vivo fate analysis of HFSCs revealed that the DNA damage response in HFSCs causes proteolysis of type XVII collagen (COL17A1/BP180), a critical molecule for HFSC maintenance, to trigger HFSC aging, characterized by the loss of stemness signatures and by epidermal commitment. Aged HFSCs are cyclically eliminated from the skin through terminal epidermal differentiation, thereby causing hair follicle miniaturization. The aging process can be recapitulated by Col17a1 deficiency and prevented by the forced maintenance of COL17A1 in HFSCs, demonstrating that COL17A1 in HFSCs orchestrates the stem cell-centric aging program of the epithelial mini-organ.

Just now realizing that COL17A1 stands for  type XVII collagen. So this is a type of collagen we are talking about here. 

More on the possibility it could regenerate thinning hair 

https://elifescience.../articles/26635