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Did you know the psoriasis genes can enhance wound healing?

Faster wound healing, the bright side of psoriasis

Every time Marvel’s Wolverine releases his claws, they cut through his skin. We assume it causes him pain, because it’s pretty obvious that even Wolverine is not immune to pain. But thanks to his “healing factor”, Wolverine doesn’t have to worry too much about injuries. There are even instances where he inflicts injuries on himself to get out of tough situations.

The X-Men might have sprung out of the creative mind of Stan Lee, but the premise behind the idea of mutants is not as far-fetched as you might think. The possibility of acquiring ‘the X gene’, and its associated superhuman powers might be impossible, but procuring a single mutation that could offer us with an inkling of a mutant power is quite probable. There are people among us that have a Wolverine-like ability to heal wounds. However, their ‘power’ comes with a price, in the form of a skin disease called psoriasis. 

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Psoriasis is a condition characterized by chronic inflammation of the skin. It’s an autoimmune disease, where the cells in our immune system which are responsible for protecting us against pathogens, instead start attacking normal, healthy cells. It’s actually this autoimmune attack that gives people with psoriasis their Wolverine-ish ability to heal wounds. The overactive immune system signals skin cells, called keratinocytes, to divide faster than normal. This comes in handy to heal a cut or a scrape, but unfortunately also leads to the build-up of dead skin at psoriatic lesions.

Two of the genes that increase the risk of psoriasis do so by influencing skin cell biology. The outer most layer of our skin serves as a protective barrier against the outside world. The LCE3D gene encodes a protein necessary for repairing the barrier layer of our skin. LCE3 proteins are not found in normal cells, but are found in high abundance after injury or inflammation to the skin. In an artificial skin model, these LCE3 ‘repair’ proteins were shown to be stimulated by the kinds of cytokines (messenger molecules) that are typically found in people with psoriasis. The rs4112788 variant of the LCE3D gene appears to affect LCE3 protein levels. Individuals with this variant have an increased risk of psoriasis. Scientists speculate that this version of LCE3D may affect the properties of the barrier layer, making the skin more susceptible to psoriasis.

The rs1801133 variant in the MTHFR gene is also linked to the risk of psoriasis. It also influences how difficult the symptoms of the disease will be to manage. The MTHFR gene gives instructions to make an enzyme that controls the levels of folic acid or vitamin B9, which is essential to copying our DNA. The MTHFR enzyme is also involved in processing of a toxic substance called homocysteine. People with rs1801133 make much less enzyme, so their folic acid levels are lower than normal. Slowing down the process of DNA copying also slows down the generation of new cells. This is especially relevant to people with psoriasis, because their skin cells grow faster than normal. This might explain why patients with the altered version of MTHFR often display milder symptoms of the disease. However, lower MTHFR levels also lead to homocysteine accumulation, which is associated with an increased risk for heart disease.

It’s easy enough to imagine how these healing factors affect a fictional character like Wolverine. However, even after several decades of research, scientists are far from uncovering the actual cause of psoriasis. The hope is that future studies will determine exactly how psoriasis-associated genes interact with external triggers of flare ups, so the symptoms of psoriasis may be better managed. Until then, perhaps you can simply focus on the brighter side of inheriting psoriasis – a Wolverine-like ability to heal wounds.

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