Abstract

This short review summarizes the localization and effects of the plant lectin soybean agglutinin (SBA) on the injured and non-injured organ-cultured rat corneal endothelium. Although the tissue exists as a non-cycling monolayer on the posterior corneal surface a circular freeze injury promotes wound repair as cells initiate DNA synthesis, mitosis and migration. As a result, by 24 h post-injury, endothelial cells express a surface protein that binds SBA in a diffuse punctate pattern, which by 48 h after injury, becomes confined to the cell periphery. As healing proceeds, SBA binding dramatically declines, such that, only scattered binding is observed by 72 h after wounding. In non-injured organ-cultured endothelia, weak SBA binding appears 24 h after explanation but becomes prominently detected around the cell periphery by 48 h. Incubating injured or non-injured endothelia in SBA leads to alterations in their cellular appearance due to the fact that lectin exposure results in the disruption of the actin cytoskeleton. Although this does not affect migration, treatment with either SBA or N-acetylgalactosamine (the SBA binding sugar) does interfere with the reestablishment of cell–cell contact. It is postulated that the surface protein that binds SBA is expressed during conditions that are stressful to the tissue. During organ-culture the protein's appearance suggests a cellular response to explantation in order to enhance or maintain monolayer integrity. In wound repair its appearance may serve to establish preliminary cell–cell contact during the restoration of the endothelial monolayer.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call