The team of researchers focused on the outmost layer of skin: the stratum corneum. It protects deeper layers from drying out or getting infected, and it’s also our first line of defense against UV radiation.
They found that beyond the well-documented DNA damage and cancer risk, UV rays also change the way the outermost skin cells hold together and respond to strain.
The researchers subjected samples of human tissue to varying doses of UVB radiation. (UVB is the range of ultraviolet wavelengths that are largely absorbed by the epidermis and do not penetrate to deeper layers.) Then they tested the mechanical limits of the samples by putting them under different kinds of stress until they tore.
We’ve all experienced the sensations of dryness, stiffness, or chapping after washing our hands with harsh soap, sitting by a space heater or under the air conditioning vent, or spending too long in the sun. Now we can begin to understand the mechanical properties behind those sensations. This is the first time that such methods have been applied to the study of skin.
Our body’s outermost stratum corneum defensive layer has a “brick-and-mortar” structure. The “bricks” in this model are dead cells called corneocytes, which are filled with a matrix of keratin filaments. Our skin’s rigidity - its ability to resist deformation under pressure - is due largely to the bonds between these strands of protein. The researchers were surprised to find that while the keratin was structurally changed by UVB exposure, the stiffness of the tissue wasn’t affected. When the skin samples were mounted onto opposing grips and pulled apart, samples with greater UVB exposure were just as resistant.
The “mortar” of skin defense, on the other hand, took a beating from the UV rays. Between the corneocytes is a layer of lipids—fatty, waxy substances that hold the skin cells together and keep water from getting though. In a process called bulge testing, thin strips of skin were mounted over the opening of a cavity filled with pressurized water so they ballooned outward. The team found that UV exposure increased the tissue’s tendency to absorb water and loosened the bonds between the lipids, making it more likely to tear under pressure. This means that sun-damaged skin is more prone to cracking and chapping, leaving deeper layers vulnerable to infection.
In another technique borrowed from materials science, the researchers used a double cantilever beam model to test the cohesive properties of skin. Imagine fused restaurant chopsticks being pried open, but with a tissue sample glued into the region that gets torn apart. UV damage made the individual corneocytes separate more easily, especially in deeper layers of the stratum corneum.
This result suggests that another component of the “mortar,” proteins called corneodesmosomes, were also being damaged. These proteins are crucial to desquamation - the process of shedding dead skin cells, which allows us to replace the entire stratum corneum every two to four weeks. While the long-term impact of UV exposure on the desquamation mechanism has not been studied yet, damage to corneodesmosomes could mean deeper, lasting damage to the skin’s protective abilities.
This story is reprinted from material from Standford Engineering, with editorial changes made by Materials Today. The views expressed in this article do not necessarily represent those of Elsevier. Link to original source.