Sliding of the epithelium in experimental corneal wounds.
The corneal epithelial cell has a unique sliding capability. The epithelial cell spreads and migrates in an amebic fashion without mitotic activity when the continuity of the epithelium is broken. This movement is demonstrated both in vivo and in vitro. Prompt sliding for sealing the wound defect is apparently the first step of the wound healing of the superficial cornea. Cut edges of collagen fibers show no sign of activity towards healing the wound. The energy source of the sliding is provided mainly from stored glycogen in the epithelial cells. Sliding is inhibited by removal of glycogen from the cell or by adding glycolytic enzyme inhibitors.
D000818:Animals; D002462:Cell Membrane / Q000648:ultrastructure; D002465:Cell Movement / Q000187:drug effects; D003315:Cornea / Q000503:physiopathology / Q000648:ultrastructure; D065306:Corneal Injuries; D003896:Desmosomes / Q000648:ultrastructure; D004721:Endoplasmic Reticulum / Q000648:ultrastructure; D004847:Epithelial Cells; D004848:Epithelium / Q000201:enzymology / Q000502:physiology / Q000648:ultrastructure; D005131:Eye Injuries / Q000473:pathology / Q000503:physiopathology*; D006003:Glycogen; D006056:Golgi Apparatus / Q000648:ultrastructure; D007365:Intercellular Junctions / Q000648:ultrastructure; D007463:Iodobenzoates / Q000494:pharmacology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008626:Mercuribenzoates / Q000494:pharmacology; D008938:Mitosis; D011817:Rabbits; D012270:Ribosomes / Q000648:ultrastructure; D014945:Wound Healing
D007463:Iodobenzoates; D008626:Mercuribenzoates; D006003:Glycogen; D007770:L-Lactate Dehydrogenase