| Several aspects of the cell biology of corneal endothelial wound repair have been studied. Uninjured endothelium consists of a homogeneous G(,0) population of cells. Histochemical and autoradiographic analyses demonstrated that many cells associated with a freeze injury enter the generative cycle. This is accompanied by changes in the association of chromosomal proteins with DNA and increased synthesis of RNA. Suppression of RNA synthesis interferes with the migration of cells into the wound as well as inhibiting mitosis. Suppression of DNA synthesis prevents mitosis but not migration. Migration appears to be more significant than mitosis in the restoration of corneal transparency during short-term healing.; Scanning electron microscopy revealed the occurrence of changes in cell surface architecture. This is the first such work that has been reported for an in vivo system. The occurrence of atypically dividing cells has been documented.; It has been demonstrated that although corneal endothelium and lens epithelium are both bathed by the aqueous humor, the mechanism(s) that control proliferation in each differ. Unlike lens epithelium, corneal endothelial growth is independent of pituitary regulation and does not respond to growth hormone dependent factors such as somatomedin - C. Growth regulation in this tissue appears to be cell density dependent.; In an effort to secure sufficient numbers of cells for future biochemical studies, tissue culture of three types of endothelium (frog, rabbit and human) have been successfully initiated. |
