Hyalocytes represent the major cell type present in the cortical tissue layer of the vitreous and are a type of connective tissue macrophage. Hyalocytes in culture produce hyaluronic acid, a process which is stimulated by testosterone and 17-alpha-estradiol, hormones which have been identified in vitreous and which are known to stimulate hyaluronic acid synthesis in other tissues. Macrophages from different sources exhibit functional heterogeneity. They may adapt to their surroundings by changing their metabolic characteristics through an amplification of enzymatic activities already present. The present application has two main goals: 1. Compare the properties of vitreous hyalocytes and peritoneal macrophages (mouse, rat) in order to determine the similarities and differences between the two types of macrophages. We have already shown that macrophages (peritoneal, alveolar) can produce hyaluronic acid. We will determine whether peritoneal macrophages in culture respond to hormones as do hyalocytes. The cell surfaces of the two macrophage types will be studied by comparing their 125I-lectin binding specificities. Cells will also be labelled with (3H)-glucosamine, and the cell surface-associated glycosaminoglycans and glycoproteins compared. The capacity of peritoneal macrophages to produce the inhibitor of endothelial cell growth, as hyalocytes apparently do, will also be analyzed. Unstimulated peritoneal macrophages do not divide in culture, while hyalocytes apparently have a slight capacity to divide. The capacity of each cell type to incorporate (3H)-thymidine into DNA will be compared. 2. Studies on hyaluronic acid synthesis by hyalocytes will be continued. The presence of steroid receptors will be determined. The question as to whether or not vitreous hyaluronic acid synthesis occurs via lipid-linked intermediates and the possible obligatory requirements for protein synthesis (as is the case for sulfated glycosaminoglycans) will also be studied. Hyalocytes may represent a macrophage which adapts to its vitreous environment by amplification of the capacity to produce connective tissue macromolecules.