ULTRASTRUCTURAL AND IMMUNOCYTOCHEMICAL STUDIES OF SMOOTH-MUSCLE CELLSIN IRIS ARTERIOLES OF RATS WITH EXPERIMENTAL AUTOIMMUNE UVEORETINITIS

In this study, we report on the ultrastructural and immunocytochemical changes that occur in smooth muscle cells of iris arterioles in S-ant igen-induced experimental autoimmune uveoretinitis (EAU). The inflamma tory phase (8-10 days postimmunization) was marked by infiltration of lymphocytes and polymorphonuclear leukocytes and monocytes in the iris stroma and perivascular tissue. Smooth muscle cells became hypertroph ic with an 11.5-fold average increase in cell volume compared with con trol cells. In some of the cells, there was a marked increase in endop lasmic reticulum, ribosomes, and Golgi elements and a concomitant decr ease in myofilaments, similar to that reported previously (Wang et al. , Curr. Eye Res. 13, 747-754, 1994). However, the majority of hypertro phic smooth muscle cells showed only a slight increase in these synthe tic organelles while retaining large amounts of myofilaments. There wa s no evidence for the migration or mitosis of the hypertrophic cells. Immunogold (IG) labeling of hypertrophic smooth muscle cells revealed changes in the immunoreactivity of several antigens. Labeling density for type I collagen increased progressively between 8 and 10 days, whi le that of decorin was slightly increased at 8 days and decreased at 1 0 days postimmunization. IG labeling for an alpha-actin isoform was si gnificantly increased during the 8-10 day period, while that of beta-a ctin isoform was decreased. The results suggest that hypertrophic smoo th muscle cells do not fully modulate to the kind of synthetic phenoty pe described in aortic smooth muscle cells. The significance of the tr ansition in immunoreactivity from alpha- to beta-actin isoform is not known although it may reflect an increased synthetic state of muscle c ells. The increased immunoreactivity of type I collagen and the change s in decorin, on the other hand, suggest that smooth muscle cells in E AU may be involved in remodeling of the extracellular matrix. (C) 1994 Academic Press, Inc.