Next time you get a paper cut, pause for a moment to consider the molecular cast of characters racing to the wound site. Proper healing requires an intricate dance between many cell types, and – for researchers and clinicians interested in tissue repair – ruling out the red herrings in the process is just as important as identifying the most-critical players.
Yesterday, Stanford stem-cell scientist and pediatric plastic and reconstructive surgeon Michael Longaker, MD, and pathologist Stephen Galli, MD, published a study in PLoS ONE showing that one class of cells, called mast cells, previously thought to be important in healing is actually not required. As Longaker explained in an e-mail to me:
Wound repair is a complex biologic process involving the interaction of many cell types to replace the lost or damaged tissue. The order in which cells arrive at the wound has been extensively studied and is generally thought to be neutrophils followed by macrophages, followed by fibroblasts, and finally mast cells. The role of each of these cells has been studied with the exception of mast cells, and very little is known about how they function in wound repair. Our study examines the role of mast cells using three mast-cell deficient mouse models. Our results indicate that mast cells do not play a significant non-redundant role during excisional wound repair.
The upshot? It appears that mast cells, which are heavily involved in allergic responses, function more like ambulance chasers than emergency responders when skin meets knife. Or, as in the case above, paper.