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Biomedical subjects

E Essner

Publications and source records attributed to E Essner.

At least 19 recordsLinked to original sources
PubMed1995

Tissue repair in the iris in experimental autoimmune uveoretinitis.

Our previous work on rats with S-antigen-induced experimental autoimmune uveoretinitis showed iris tissue changes involving infiltration of inflammatory cells, destruction of the iris architecture, and breakdown of the blood-retinal barrier. The present study reports the remarkable ability of the iris to regenerate during the postinflammatory period. The iris regenerates 50% of its architecture by Day 20 postimmunization. The number of lymphocytes and polymorphonuclear leukocyte (PMNs) was relatively high at this stage. Many capillaries showed abnormal endothelial cells. Unmyelinated nerve axons were often seen near blood vessels. The iris stroma was edematous. By Day 30, approximately 95% of the iris had regenerated, the number of lymphocytes and PMNs decreased, and the number of macrophages increased. Most capillaries looked normal and numerous axons in different stages of myelination were apparent. The stroma, the dilator muscle, and the posterior epithelium were almost completely restored. By Day 45, the iris appeared to be virtually normal. Most striking was the abundance of myelinated nerve axons located near blood vessels. Type I collagen immunoreactivity in vascular endothelial cells increased from Day 20 to Day 60 postimmunization, suggesting that blood vessel endothelial cells may play a role in collagenization of the iris stroma.

Animals↗
PubMed1994

Ultrastructural and immunocytochemical studies of smooth muscle cells in 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-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.

Actins↗
PubMed1994

Ultrastructural and immunocytochemical studies of iris vessels in rats with experimental autoimmune uveoretinitis.

In this study, we describe the ultrastructural and immunocytochemical changes that occur in the iris of rats with experimental autoimmune uveoretinitis (EAU). General changes include perivascular infiltration of inflammatory cells, followed by hemorrhage and extensive tissue destruction. Alterations in the iris epithelium were also noted. A breakdown in the blood-iris barrier was demonstrated in some vessels at the peak of inflammation; peroxidase reaction product was seen in the basement membrane and perivascular spaces. We found that, in inflamed iris vessels, endothelial cells and smooth muscle cells become hypertrophic and show increased amounts of synthetic organelles. This finding is similar to our previous observations on endothelial cells and smooth muscle cells in retinal vessels in EAU. In addition, as was reported in the retinal vascular basement membrane in EAU, there is an increase in immunoreactivity of several extracellular matrix molecules in the iris vascular basement membrane; during inflammation, there is a significant increase in immunoreactivity of collagen types I and III, entactin, fibronectin, and laminin. Activated endothelial cells and smooth muscle cells are likely to be involved in the synthesis of certain of these matrix molecules.

Animals↗
PubMed1994

Differential localization of type IV collagen in Bruch's membrane of the eye: comparison of two polyclonal antibodies.

The ultrastructural localization of type IV collagen in the basal lamina of the retinal pigment epithelium (RPE) and choriocapillary endothelium (CCE) of the rat eye was studied using a pre-embedding immunoperoxidase and a post-embedding immunogold method. Antibodies to type IV collagen from human placenta and from murine Engelbreth-Holm-Swarm (EHS) sarcoma were used with both methods. In the preembedding method, both antibodies were localized to the basal lamina of the RPE and CCE. In the postembedding method, antibody to EHS tumor collagen was also localized to both basal laminae. However, when the latter method was used with antibody to placental collagen, much less labeling was seen in the basal lamina of the RPE compared with that in the CCE. The findings suggest that in the basal lamina of the RPE (but not the CCE), the strongly immunogenic 7S domain of type IV collagen is inaccessible to antibodies directed against this protein. This effect may be due to masking of the 7S domain by other components or to a conformational change in the collagen molecule.

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PubMed1992

Ultrastructural immunocytochemical localization of chondroitin sulfate proteoglycan in Bruch's membrane of the rat.

Two monoclonal antibodies (Mab 4D5 and 2D6) raised against the core protein of a basement membrane chondroitin sulfate proteoglycan from Reichert's membrane of the rat, were used for ultrastructural immunoperoxidase localization of this protein in Bruch's membrane of the rat. Immunoreactivity for both antibodies was found in the basal lamina (basement membrane) of the choriocapillary endothelium and retinal pigment epithelium, in collagen fibers in the collagenous zones, and surrounding the elastic layer.

Animals↗
PubMed1991

Breakdown of the blood-retinal barrier in S-antigen-induced uveoretinitis in rats.

Experimental autoimmune uveoretinitis was induced in Lewis rats by footpad injection of purified, bovine retinal soluble antigen (S-antigen) with complete Freund's adjuvant. Control animals received adjuvant only. At the peak of ocular inflammation the animals received an intravenous injection of the tracer horseradish peroxidase, and the eyes were removed and processed for peroxidase cytochemistry. A breakdown of the blood-retinal barrier occurred at the level of the retinal venules. Peroxidase reaction product was demonstrable in the interendothelial tight junctions and in the perivascular spaces. Heavy infiltration of inflammatory cells was also found in and around the venular wall. The endothelial cells of venules and capillaries were hypertrophied and showed swollen endoplasmic reticulum and Golgi apparatus as well as increased numbers of ribosomes and cytoplasmic fibrils; pericytes and smooth-muscle cells showed a similar synthetic phenotype and the basal lamina of these cells was thickened.

Animals↗
PubMed1991

Increased immunoreactivity of collagen types I, III and V, fibronectin and TGF-beta in retinal vessels of rats with experimental autoimmune uveoretinitis.

The immunoreactivity of types I, III and V collagen, fibronectin and transforming growth factor-beta (TGF-beta) was studied by an immunogold labeling method in retinal vessels of rats with experimental autoimmune uveoretinitis (EAU) induced by retinal S-antigen. The basal lamina of retinal capillaries in normal rats showed low immunoreactivities for the extracellular matrix components and TGF-beta. However, at the peak of inflammation (day 13-16 postimmunization), labeling of all three types of collagen and fibronectin increased considerably in the basal lamina of retinal vessels. TGF-beta immunoreactivity was detected mainly in the vascular endothelium and the pericytes. The results suggest that TGF-beta synthesized by the endothelial cells and pericytes may regulate the synthesis and composition of extracellular matrix components in the vascular basal lamina during the course of EAU development.

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PubMed1990

Immunogold localization of basement membrane molecules in rat retinal capillaries.

Vascular basement membrane contains laminin, fibronectin, proteoglycan and collagens. These molecules have been identified in various tissues by immunolabeling methods and biochemical analyses. We have previously localized laminin, fibronectin and type IV collagen to the basement membrane of rat retinal vessels at the ultrastructural level using an immunoperoxidase method. In this study, we use an immunogold method to re-examine the distribution of these molecules and also to study the localization of heparan sulfate proteoglycan and types I, III and V collagen in the retinal capillary basement membrane. Gold labeling for laminin, type IV collagen and proteoglycan were found diffusely on the basement membrane of the endothelium and pericyte, while that for fibronectin and type V collagen was spotty and variable and that for types I and III collagen was negligible. The segment of basement membrane between the endothelial cell and pericyte appeared less reactive to anti-laminin and anti-type IV collagen than the membrane between the pericyte and perivascular neuroretina. The immunogold method may be useful in quantitative studies of thickened basement membranes under abnormal conditions.

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PubMed1988

Ultrastructural and permeability characteristics of retinal vessels in stroke-prone spontaneously hypertensive rats.

The ultrastructure and permeability of retinal arterioles, venules, and capillaries located near the optic disc of stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats were studied using electron microscopy and tracer cytochemistry. A variety of structural changes were observed in arterioles of SHRSP. They include (1) narrowing of the lumen due to smooth muscle hyperplasia and/or fragmentation and thickening of the basal lamina, (2) fusiform aneurysms containing degenerated smooth muscle cells and reduplicated basal lamina, and (3) the presence of microfilament bundles under the luminal surface of the endothelium. In addition, the wall of venules was thickened due to accumulation of basal lamina material. Many capillary pericytes were also degenerated. Retinal vessels of age-matched normotensive rats did not show such changes. In SHRSP, after injection of peroxidase, extravasation of tracer was seen occasionally in retinal capillaries and in the central retinal vein at the optic nerve head. No changes in vascular permeability were observed in the normotensive rats.

Animals↗
PubMed1988

Immunocytochemical localization of laminin, type IV collagen and fibronectin in rat retinal vessels.

Laminin, type IV collagen and fibronectin have been identified as major components of the basement membrane (basal lamina) in various tissues. These antigens have also been identified in retinal vessels by light microscopic immunofluorescence but their precise location could not be determined at this level of resolution. In this study, we examined the localization of these constituents at the ultrastructural level using the protein A-immunoperoxidase technique. The basal lamina of all retinal capillaries, arterioles and venules was immunostained after exposure to antisera against laminin, type IV collagen and fibronectin. Staining was localized to the lamina densa, which appeared as a single or double layer. Immunostaining for fibronectin showed the weakest activity. The reaction was also seen in discrete patches between endothelial cells and pericytes. The inner limiting membrane of the retina was also reactive for laminin and type IV collagen but not for fibronectin. The results indicate that laminin, type IV collagen and fibronectin are components of the basal lamina in all types of retinal vessels. The presence of fibronectin at the endothelial-pericyte interface suggests that this protein may promote adhesion between cells and thus help to maintain the integrity of the vessel wall.

Animals↗
PubMed1988

Retinal dystrophy in Wistar-Furth rats.

A form of retinal degeneration in the Wistar-Furth strain of rat is described. The changes observed was classified as either mild or severe, depending on the severity of the dystrophy seen by light and electron microscopy. In the mild stage, there was a slight decrease in the number of photoreceptor nuclei in the outer nuclear layer (ONL) and there were pyknotic nuclei in the inner nuclear layer. A few photoreceptor outer and inner segments showed focal swellings. The basal infoldings of the retinal pigment epithelium (RPE) were distributed irregularly, creating spaces that contained collagen-like fibrils. However, the interepithelial tight junctions remained impermeable to intravenously injected peroxidase. In severely dystrophic retinas, there was a further decrease in the width of the ONL, and the photoreceptor outer and inner segments were degenerated. In extreme cases, the photoreceptor cell disappeared completely and the inner retina abutted the RPE. Further changes were also noted in the basal membrane of the RPE; in some regions the membrane was totally flat while in others it formed exaggerated infoldings. In addition, the RPE was frequently vascularized by vessels that originated from the retina. The endothelium of those intra-RPE vessels located near Bruch's membrane was frequently fenestrated. Alterations also occurred in the retinal capillaries; some were degenerated, while others showed increased tortuosity or focal thickenings of the basal lamina. In addition, there were focal increases in the amount of stroma between Bruch's membrane and the choriocapillaris.

Animals↗
PubMed1987

Luminal vesicles in endothelial cells of retinal and iridial vessels of the rat.

Endothelial vesicles on the luminal front of retinal and iridial vessels were studied by perfusion fixation after intravenous injection of peroxidase, and by perfusion fixation of glutaraldehyde with tannic acid or ruthenium red. Many luminal vesicles contained peroxidase reaction product after intravenous injection of peroxidase, but were virtually empty after perfusion fixation. Both tannic acid and ruthenium red delineated the majority of luminal vesicles, singular or in clusters, surface-associated or "free" in the cytoplasm. Only a few free vesicles were unlabeled by the dye. No transendothelial channels were seen. The results suggest that most of the vesicles on the luminal front of endothelial cells are continuous with the cell surface at the time of fixation. The function of these vesicles is not fully understood; some appear to be involved in endocytosis of macromolecules from the vascular lumen.

Animals↗
PubMed1987

Investigations on circumferential microfilament bundles in rat retinal pigment epithelium.

The presence of contractile proteins in normal rat retinal pigment epithelium has been studied using fluorescence and electron microscopy. Investigations using the F-actin binding toxin, phallacidin, coupled to the fluorochrome nitrobenzoxadiazole, revealed a band of fluorescence at or near the cell membrane. Immunofluorescent observations with anti-myosin and anti-alpha-actinin antisera gave similar results. Electron microscopy employing glutaraldehyde-8% tannic acid fixation revealed the presence of a circumferential microfilament band beneath the pigment epithelial apical surface that is closely associated with the plasma membrane and junctional complexes. Freeze-fracture studies confirmed the relationship of this band to the junctional complexes. The microfilament band measures approximately 0.5 micron +/- 0.2 micron in width and is composed of numerous 6 to 7 nm filaments. Some microtubules are seen in regions around the band, but no organelles appear to be associated with this structure. In en face sections through the zonula adherens, the circumferential microfilament band is associated with 30-nm electron-dense particles that are bound to the internal side of the membrane. Morphological evidence suggests that these may serve in anchoring the band to the membrane and assist in aligning the microfilament bands of adjoining cells. In the subapical cytoplasm, a microfilament bundle network was detected that interfaced with the circumferential microfilament band. In some cases, pigment epithelium was incubated in media-199 containing 25 to 50 ng/ml phallacidin prior to fixation. Circumferential microfilament bands of tissues treated in this manner exhibited a striated appearance.

Actin Cytoskeleton↗
PubMed1987

An electron microscopic study of retinal degeneration in Sprague-Dawley rats.

Retinal degeneration in untreated, female Sprague-Dawley rats was studied by electron microscopy and horseradish peroxidase tracer technique. The degeneration appeared to have started at a very young age. The severity of the defect varied from a decrease of photoreceptor nuclei to total loss of receptor cells and the pigment epithelium. In mild degeneration some regions of the retinal pigment epithelium became bilayered and the basal plasma membrane became flattened or formed elaborate infoldings. Breaks in Bruch's membrane occurred in severe degeneration. Degeneration of the pigment epithelium allowed permeation of tracer material from the choroid into the retina.

Animals↗
PubMed1986

Actin, myosin, and laminin localization in retinal vessels of the rat.

Actin, myosin, and laminin have been localized in retinal vessels of normal rats by fluorescence microscopy. Actin was localized with the fluorescent F-actin binding toxin nitrobenzoxadiazole phallacidin (NBD-Ph). Indirect immunofluorescence was used to localize myosin and laminin. In addition, laminin localization was also performed with the Protein A-horseradish peroxidase (PA-HRP) method. NBD-Ph staining gave strong fluorescence in both retinal capillaries and larger vessels. Anti-myosin fluorescence could also be observed in trypsin digests of the retinal vasculature. Strong fluorescence of PA-HRP reaction product could be detected in the walls of vessels exposed to anti-laminin antibody. Actin distribution in vessels of the RCS rat with inherited retinal degeneration (retinal dystrophic RCS rat) was also studied. After exposure to NBD-Ph, all capillaries showed fluorescence. However, it was more intense in many of the capillaries in the outer retina, which also appeared morphologically abnormal. Electron microscopy of retinal capillaries fixed in 2.5% glutaraldehyde containing 8% tannic acid revealed numerous microfilaments in the pericyte cytoplasm and some in the basal portion of endothelial cells. In pericytes, these microfilaments are in close association with the endothelial side of the cell. Tangential sections through this region indicate that these filaments may be anchored to the membrane at this site.

Actins↗
PubMed1986

Surface-associated vesicles in retinal arterioles and venules.

The surface-associated vesicles in retinal arterioles and venules were studied after fixation in glutaraldehyde-tannic acid or after intravitreal injection of peroxidase or lactoperoxidase. The vesicles were concentrated along the abluminal (basal) surface of the endothelial cells and along the plasma membranes of smooth muscle cells in arterioles and of pericytes in post-capillary venules. They were rarely encountered in the deeper regions of these cells. In perpendicular sections through the cell surface the majority of vesicles were in continuity with the plasma membrane whereas in tangential sections, they appeared to lie "free" in the cytoplasm. All such vesicles were labeled after exposure to tannic acid or to the heme-proteins. Peroxidase-reaction product was never seen in the lumen of the vessels. These observations suggest that the surface vesicles in endothelial cells, smooth muscle cells and pericytes are invaginations of the plasma membrane and are thus not involved in the transcytosis or endocytosis of proteins. The vesicles in the latter two cell types may be involved in some aspect of contractility rather than pinocytosis.

Animals↗
PubMed1986

Diffuse cytoplasmic staining of retinal capillary endothelium.

The distribution of several hemeprotein tracers in retinal capillaries of Wistar-Furth rats was studied by electron microscopic cytochemistry after incubation in 3,3'-diaminobenzidine. Diffuse cytoplasmic reaction product was frequently observed in the endothelial cells after intravenous injection of horseradish peroxidase (HRP) or lactoperoxidase (LP), or after perfusion of HRP. Occasionally, pericytes were also diffusely stained. In contrast, injection of microperoxidase, catalase, or hemoglobin did not cause diffuse staining. The diffuse staining was similar with HRP types II, VI, and VIII, and at concentrations of 2.5, 5, and 10 mg/100 g body weight. Despite the staining, the blood-retinal barrier remained intact. The findings indicate that HRP and LP are capable of causing diffuse nonspecific staining of retinal capillary endothelial cells, even at relatively low concentrations. Since these tracers are frequently used in studies of the blood-retinal barrier, the results of such studies should be interpreted with caution.

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