Skin Is Repaired by Zipper Mechanism
The details of wound repair and prevention are coming to light.
A cut in the skin starts an automatic repair process with many cellular players. In “Zip me up! Zooming into wound repair,” Science Daily reports on new findings from the Goethe-Universität Frankfurt am Main on how the “orchestra of healing” plays its intricate performance. The researchers recorded “an enormous amount of data that surpasses all previous studies of this kind,” and found a zipper-like mechanism at work. Behold your body’s sewing machine:
In order to prevent death by bleeding or infection, every wound (skin opening) must close at some point. The events leading to skin closure had been unclear for many years. Mikhail Eltsov (GU) and colleagues used fruit fly embryos as a model system to understand this process. Similarly to humans, fruit fly embryos at some point in their development have a large opening in the skin on their back that must fuse. This process is called zipping, because two sides of the skin are fastened in a way that resembles a zipper that joins two sides of a jacket.
The scientists have used a top-of-the-range electron microscope to study exactly how this zipping of the skin works. “Our electron microscope allows us to distinguish the molecular components in the cell that act like small machines to fuse the skin. When we look at it from a distance, it appears as if skin cells simply fuse to each other, but if we zoom in, it becomes clear that membranes, molecular machines, and other cellular components are involved,” explains Eltsov.
Indeed, the electron micrographs show parts the bear an uncanny resemblance to an actual zipper. Or, perhaps Velcro.
As a first step, as the scientists discovered, cells find their opposing partner by “sniffing” each other out. As a next step, they develop adherens junctions which act like a molecular Velcro. This way they become strongly attached to their opposing partner cell. The biggest revelation of this study was that small tubes in the cell, called microtubules, attach to this molecular Velcro and then deploy a self-catastrophe, which results in the skin being pulled towards the opening, as if one pulls a blanket over.
This all happens very quickly. When only 5-10 cells have found their partners, the skin “already appears normal.” How did this evolve? They couldn’t say, exactly. “The scientists were astonished to find that microtubules involved in cell-division are the primary scaffold used for zipping, indicating a mechanism conserved during evolution.”
Skin So Tough
Another study, this one from UC Berkeley, found out new things about collagen, the protein that makes up much of human skin. This protein is largely responsible for keeping skin from tearing in the first place:
When weighing the pluses and minuses of your skin add this to the plus column: Your skin – like that of all vertebrates – is remarkably resistant to tearing. Now, a collaboration of researchers at the U.S. Department of Energy (DOE)’s Lawrence Berkeley National Laboratory (Berkeley Lab) and the University of California (UC) San Diego has shown why.
Making good use of the X-ray beams at Berkeley Lab’s Advanced Light Source (ALS), the collaboration made the first direct observations of the micro-scale mechanisms behind the ability of skin to resist tearing. They identified four specific mechanisms in collagen, the main structural protein in skin tissue, that act synergistically to diminish the effects of stress.
The team found that collagen is strong because its fibrils “rotate, straighten, stretch and slide” when applied stress tries to cause a tear in the skin. For low strains, there’s elastin, another protein that works with collagen in the dermis. Because of the material properties of these proteins, skin can automatically absorb much strain without tearing. “Our study is the first to model and directly observe in real time the micro-scale behavior of the collagen fibrils associated with the skin’s remarkable tear resistance,” one of the researchers said.
What they demonstrated instead is that the tearing or notching of skin triggers structural changes in the collagen fibrils of the dermis layer to reduce the stress concentration. Initially, these collagen fibrils are curvy and highly disordered. However, in response to a tear they rearrange themselves towards the tensile-loading direction, with rotation, straightening, stretching, sliding and delamination prior to fracturing.
Studying this mechanism inspired them to think about what bioengineers could learn from it:
“Natural inspiration is a powerful motivation to develop new synthetic materials with unique properties,” Ritchie says. “For example, the mechanistic understanding we’ve identified in skin could be applied to the improvement of artificial skin, or to the development of thin film polymers for applications such as flexible electronics.”
In sum, your body does its best to resist a wound. But when it occurs, the sewing machines know how to zip you back up.
This is a great example of how using an intelligent design approach to study something as close as the back of your hand can lead to intelligent design of artificial materials. Darwinism has nothing to say. These mechanisms were “conserved [unevolved] during evolution.” If something is unevolved during evolution, then evolution is useless; it can’t account for the origin of the mechanism, nor its persistence. The usefulness of intelligent design, by contrast, is readily apparent, inspiring, and productive.