Osmotic gradient is just the tonic for wounded epithelia

E pithelial layers protect organisms from their external environment, and any damage to these tissues must therefore be repaired as quickly as possible. Wound repair is generally thought to be initiated by intrinsic cues, such as changes in the structure or mechanics of damaged tissues. But Gault et al. reveal that extrinsic signals can also trigger tissue repair. In particular, differences between the osmolarity of zebrafi sh tissues and their external environment can stimulate wound closure by inducing epi-thelial cell migration (1). Zebrafi sh live in fresh water, which has an osmolarity much lower than that of the animal's interstitial fl uids. Philipp Nietham-mer and colleagues at Memorial Sloan Ket-tering Cancer Center in New York previously demonstrated that the drop in interstitial osmolarity that occurs when zebrafi sh tailfi ns are wounded and exposed to their environment stimulates the recruitment of leukocytes that mediate the tissue's inflammatory response over the following few hours (2). Niethammer wondered whether osmolar-ity differences might also regulate the more immediate wound response of the tailfi n epithelial cells, which quickly act to seal any holes in the tissue. " Because epi-thelial barriers are so important for protecting the organism, it's essential that wound responses are initiated within seconds of the injury, " Niethammer explains. Niethammer and colleagues, led by post-doc William Gault, therefore examined the immediate wound response of zebrafi sh lar-vae surrounded by an isotonic, rather than a hypotonic, environment (1). " The sheet of epithelial cells didn't react to the presence of the wound, " Niethammer says. " So by abrogating the osmolarity difference between the inside and the outside of the fi sh, the fi sh didn't know it was injured. " The zebrafi sh tailfi n epithelium consists of two layers of cells, an inner basal layer attached to the underlying basement membrane and an outer, suprabasal layer that acts as the tissue's permeability barrier. Gault et al. found that, after injury in hypo-tonic media, suprabasal cells assembled a multicellular actomyosin " purse string " around the wound margin, while the basal cells migrated as a sheet toward the center of the wound, apparently dragging the suprabasal cells along for the ride. In isotonic media, the suprabasal cells still formed a purse string, but the basal cells didn't migrate and therefore failed to close the wound and restore the epithelial barrier. " So there are different wound closure mechanisms in the …