title: Ultrastructural and immunocytochemical studies of smooth muscle cells in iris arterioles of rats with experimental autoimmune uveoretinitis.
abstract: In this study, we report on the ultrastructural and immunocytochemical changes that occur in smooth muscle cells of iris arterioles in S-antigen-induced experimental autoimmune uveoretinitis (EAU). The inflammatory 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 hypertrophic with an 11.5-fold average increase in cell volume compared with control cells. In some of the cells, there was a marked increase in endoplasmic reticulum, ribosomes, and Golgi elements and a concomitant decrease in myofilaments, similar to that reported previously (Wang et al., Curr. Eye Res. 13, 747-754, 1994). However, the majority of hypertrophic smooth muscle cells showed only a slight increase in these synthetic organelles while retaining large amounts of myofilaments. There was 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, while that of decorin was slightly increased at 8 days and decreased at 10 days postimmunization. IG labeling for an alpha-actin isoform was significantly increased during the 8-10 day period, while that of beta-actin isoform was decreased. The results suggest that hypertrophic smooth muscle cells do not fully modulate to the kind of synthetic phenotype described in aortic smooth muscle cells. The significance of the transition in immunoreactivity from alpha- to beta-actin isoform is not known although it may reflect an increased synthetic state of muscle cells. The increased immunoreactivity of type I collagen and the changes in decorin, on the other hand, suggest that smooth muscle cells in EAU may be involved in remodeling of the extracellular matrix.
authors.affiliation: Kresge Eye Institute, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.
authors.forename: J
authors.initials: J
authors.lastname: Wang
authors.forename: E
authors.initials: E
authors.lastname: Essner
authors.forename: H
authors.initials: H
authors.lastname: Shichi
mesh_terms: D000199:Actins / Q000032:analysis; D000818:Animals; D001160:Arterioles / Q000276:immunology / Q000473:pathology; D001327:Autoimmune Diseases / Q000276:immunology / Q000473:pathology*; D003094:Collagen / Q000032:analysis; D058575:Decorin; D016326:Extracellular Matrix Proteins; D005260:Female; D006984:Hypertrophy / Q000473:pathology; D007106:Immune Sera / Q000276:immunology; D007150:Immunohistochemistry; D007498:Iris / Q000098:blood supply*; D016253:Microscopy, Immunoelectron; D009130:Muscle, Smooth / Q000737:chemistry / Q000276:immunology / Q000473:pathology*; D011509:Proteoglycans / Q000032:analysis; D051381:Rats; D011917:Rats, Inbred Lew; D012173:Retinitis / Q000276:immunology* / Q000473:pathology; D014605:Uveitis / Q000276:immunology* / Q000473:pathology
chemical_list: D000199:Actins; D058575:Decorin; D016326:Extracellular Matrix Proteins; D007106:Immune Sera; D011509:Proteoglycans; D003094:Collagen