Today, Matthew Wyczalkowski at Washington University in St Louis and a couple of pals say they’ve found a third healing mechanism that closes embryonic wounds by as much as 50 percent in the first 30 seconds after the injury occurs.
The two known wound healing mechanisms have been studied for some years. In the first of these, the wound closes via a purse-string mechanism using the same mechanism responsible for muscle contraction. This relies on biological cables called actins that contract when pulled by biological motors called myosins.
In embryonic wound healing, a cable of actin forms around the edge of the wound which myosins then tighten. This closes the wound like a purse string.
The second known mechanism is a kind of zippering effect that kicks into action after the purse-string phase has closed the wound. It starts with the formation of tiny ribs of actin on each side of the wound which then link together like a zip, finally sealing the damage.
Both these mechanisms have been studied in detail but Wyczalkowski and co were intrigued by anecdotal evidence that embryonic wounds can shrink dramatically in the first few seconds after they occur.
That’s too quickly for either of the two known mechanisms which rely on the growth of actin fibres and myosin motors, something that takes time. Clearly, if these reports were true, some other mechanism had to be involved.
To find out, they created circular wounds in more than 50 Leghorn chicken embryos incubated for 21 days and then watched to see what happened.
To their surprise, these wounds shrank dramatically in the first 30 seconds after they occurred, some by up to 50 per cent in surface area. They used a fluorescent staining technique to show that actomyosin was again involved in this contraction.
But in this case, the staining showed the actomyosin at work in a thick ring some three or four cells deep around the perimeter of the wound. That’s in contrast to the purse string effect, which occurs in a thin cable that grows around the edge of the wound.
Wyczalkowski and co think that this contraction occurs inside individual cells, which in normal circumstances contain a kind of scaffolding structure made of actomyosin. They suggest that wound formation releases calcium ions into the nearby environment and this immediately triggers the contraction of any actomyosin in the vicinity.
When the actomyosin in cell scaffolding shrinks, it reduces the volume of the cell. And when this happens around the damage, it causes the wound to shrink too.
Wyczalkowski and co tested their idea in a computer model of wound healing which suggested that their new mechanism was indeed viable.
That’s an interesting discovery. It means that wound healing in chicken embryos is a three-stage process. In the first stage, the wound shrinks by up to 50 per cent in the first 30 seconds. It then undergoes a period of slower contraction as the purse-string effect kicks in. In the final stage, the wound zippers up. The result is a perfect scar-free repair.
That’s in stark contrast to wound healing in adults which involves the action of special cells called fibroblasts that synthesise collagen to fill in any gaps. Hence the formation of scars.
Of course, there are good reasons why adult wound healing occurs in a different way. Not least of these is that wounds in adults are exposed to germs and dirt whereas chicken embryos grow in their own clean room.
However, a better understanding of how wounds can heal without scarring could clearly be useful. Just don’t plan on any scar-free cosmetic surgery just yet.
Ref: arxiv.org/abs/1303.4784: Computational and Experimental Study of the Mechanics of Embryonic Wound Healing