page 555 from Richards et al. The brownout might give healing cells a migratory edge.
Skin cells talk to each other through gap junctions, which allow the passage of ions and small signaling molecules such as cAMP and ATP. Junctions can be made more selective—allowing fewer or smaller molecules to pass through—by a serine phosphorylation on connexin43 (Cx43), the main structural protein of gap junctions in human skin.
This phosphorylation is now shown to occur in the basal layer of skin cells within 200 μm of a wound. In cultured skin cell monolayers, dye normally spread through the junctions across 25 cells, but wounding and the subsequent protein kinase C–dependent phosphorylation of Cx43 limited the dye's reach to only 4 cells. In skin tissue, the changes probably partially seal off basal cells both from one another and from the overlying layers of cells.
Gap junctions were closed only temporarily, at a time when basal cells—which harbor the skin's stem cells—change from an anchored, stable state to a mobile one. Early gap junction communication was needed for cell migration into a wound in monolayers, as migration was inhibited if the junctions were blocked before, but not 6 h after, an injury.
The identity of the signals whose movements are later restricted by the decrease in communication are not yet known. The basal cells have plenty of the phosphorylated channels and thus may let out molecules that alert unwounded area cells of the injury. But these same phosphorylated channels may impede both the outwards flow of their own migratory signals and the inward flow of differentiation signals coming from overlying cells.