A team of researchers at Keio University (Minato, Japan), working with Imperial College London (England), used two microscopy methods to help discover the shape and binding capability of skin cells (epidermal cells). The work could someday explain how skin maintains a barrier, even when it is shedding.
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The authors of the study say their new understanding of how epidermal cells form a barrier may explain the paradox of how we can shed them without compromising our skin's integrity. It could also help us to understand what happens when it forms incorrectly, which can lead to conditions like psoriasis and eczema.
During a 24-hour period, a human loses almost five billion skin cells. It has been a challenge for scientists to explain how this shedding process can occur without there being a break in the skin barrier. Scientists have previously known the epidermis consists of a thick outer barrier of dead epidermal cells, which are constantly shedding. What they've known less about is a secondary barrier deeper below the surface in the epidermis that is made up of only a single layer of cells, which forms a much thinner, though no less important, protective barrier.
Now, the research team has discovered that the shape of the epidermal cells, combined with their ability to temporarily glue together, may explain how they form this strong barrier. They suggest that a shape of an epidermal cell is actually a flattened version of a tetrakaidecahedron—a 14-sided 3D solid made out of six rectangular and eight hexagonal sides. The authors came to their conclusion after studying skin cells in mouse models using confocal and two-photon microscopy, and developing mathematical models.
The researchers say that the epidermal cells' unique tetrakaidecahedron-like geometry means that it can always form a very tight, cohesive bond with the epidermal cells surrounding it. This is because the mix of rectangular and hexagonal sides enables the cell to always be tightly connected to the cells surrounding it.
The team also discovered that these cells manufacture proteins, which act as a temporary glue that binds the cells together in what are called tight junctions. The combination of the cells' geometry and tight junction formation means that the skin barrier can maintain its integrity, even though it is very thin. When new cells underneath form the new tight junctions, this pushes the older cells upwards towards the surface of the skin, and the older cells lose their tight junctions. In this way, the tight junction barrier in the cell sheet is always maintained.
The team suggest that malfunctions in the production of the tight junctions may be a contributing factor that explains why some people have conditions such as eczema, where the skin barrier is weakened, which leads to bacterial infiltration, inflammation, scratching, and further infection. In other cases, fails in the interlocking barrier between cells—the tight junctions—may partly explain why in psoriasis there is an overproduction of epidermal cells, causing thick patches of skin on the surface.
Next, the researchers will analyze how skin thickness is determined and how the balance between cell growth and cell shedding is maintained. Faults in this process can lead to a thickening of the skin, leading to conditions like psoriasis. The team will also determine why skin thins as we get older, providing new insights into aging, or when it thins because special treatments like steroids are administered to treat eczema.
Full details of the work appear in the journal eLife; for more information, please visit http://dx.doi.org/10.7554/eLife.19593.