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1.
Sci Rep ; 9(1): 3278, 2019 03 01.
Article in English | MEDLINE | ID: mdl-30824736

ABSTRACT

The purpose of this study was to evaluate focal damage in the retinal pigment epithelium (RPE) layer in serous retinal pigment epithelium detachment (PED) with multi-contrast optical coherence tomography (OCT), which is capable of simultaneous measurement of OCT angiography, polarization-sensitive OCT and standard OCT images. We evaluated 37 eyes with age-related macular degeneration that had serous PED. Focal RPE damage was indicated by hyper-transmission beneath the RPE-Bruch's membrane band in standard OCT images. Distribution of RPE melanin was calculated using the dataset from multi-contrast OCT. Twenty-four points with hyper-transmission were detected in 21 of the 37 eyes. Standard OCT images failed to show disruption of the RPE-Bruch's membrane band at 5 of the 24 hyper-transmission points. Conversely, multi-contrast OCT images clearly showed melanin defects in the RPE-Bruch's membrane band at all points. Areas of melanin defects with disruption of the RPE-Bruch's membrane band were significantly larger than those without disruption. The volume of intraretinal hyper-reflective foci was significantly larger in eyes with hyper-transmission than that in eyes without hyper-transmission. Multi-contrast OCT is more sensitive than standard OCT for displaying changes at the RPE-Bruch's membrane band when there are small areas of RPE damage.


Subject(s)
Angiography , Retinal Detachment , Retinal Pigment Epithelium , Aged , Aged, 80 and over , Bruch Membrane/blood supply , Bruch Membrane/diagnostic imaging , Bruch Membrane/injuries , Bruch Membrane/metabolism , Female , Humans , Male , Melanins/metabolism , Middle Aged , Retinal Detachment/diagnostic imaging , Retinal Detachment/metabolism , Retinal Pigment Epithelium/blood supply , Retinal Pigment Epithelium/diagnostic imaging , Retinal Pigment Epithelium/metabolism , Tomography, Optical Coherence
2.
Prog Retin Eye Res ; 45: 1-29, 2015 Mar.
Article in English | MEDLINE | ID: mdl-25486088

ABSTRACT

Age-related macular degeneration (AMD) is a common and devastating disease that can result in severe visual dysfunction. Over the last decade, great progress has been made in identifying genetic variants that contribute to AMD, many of which lie in genes involved in the complement cascade. In this review we discuss the significance of complement activation in AMD, particularly with respect to the formation of the membrane attack complex in the aging choriocapillaris. We review the clinical, histological and biochemical data that indicate that vascular loss in the choroid occurs very early in the pathogenesis of AMD, and discuss the potential impact of vascular dropout on the retinal pigment epithelium, Bruch's membrane and the photoreceptor cells. Finally, we present a hypothesis for the pathogenesis of early AMD and consider the implications of this model on the development of new therapies.


Subject(s)
Choroid/blood supply , Complement Activation/physiology , Complement System Proteins/physiology , Macular Degeneration/immunology , Aging/physiology , Bruch Membrane/blood supply , Complement System Proteins/genetics , Humans , Macular Degeneration/genetics , Macular Degeneration/physiopathology , Retinal Pigment Epithelium/blood supply
3.
PLoS One ; 8(3): e55667, 2013.
Article in English | MEDLINE | ID: mdl-23469166

ABSTRACT

Tissue inhibitors of metalloproteinases (TIMPs) while originally characterized as inhibitors of matrix metalloproteinases (MMPs) have recently been shown to have a wide range of functions that are independent of their MMP inhibitory properties. Tissue inhibitor of metalloproteinases-3 (TIMP-3) is a potent inhibitor of VEGF-mediated angiogenesis and neovascularization through its ability to block the binding of VEGF to its receptor VEGFR-2. To identify and characterize the anti-angiogenic domain of TIMP-3, structure function analyses and synthetic peptide studies were performed using VEGF-mediated receptor binding, signaling, migration and proliferation. In addition, the ability of TIMP-3 peptides to inhibit CNV in a mouse model was evaluated. We demonstrate that the anti-angiogenic property resides in the COOH-terminal domain of TIMP-3 protein which can block the binding of VEGF specifically to its receptor VEGFR-2, but not to VEGFR-1 similar to the full-length wild-type protein. Synthetic peptides corresponding to putative loop 6 and tail region of TIMP-3 have anti-angiogenic properties as determined by inhibition of VEGF binding to VEGFR-2, VEGF-induced phosphorylation of VEGFR-2 and downstream signaling pathways as well as endothelial cell proliferation and migration in response to VEGF. In addition, we show that intravitreal administration of TIMP-3 peptide could inhibit the size of laser-induced choroidal neovascularization lesions in mice. Thus, we have identified TIMP-3 peptides to be efficient inhibitors of angiogenesis and have a potential to be used therapeutically in diseases with increased neovascularization.


Subject(s)
Angiogenesis Inhibitors/pharmacology , Bruch Membrane/blood supply , Bruch Membrane/drug effects , Choroidal Neovascularization/prevention & control , Peptides/pharmacology , Tissue Inhibitor of Metalloproteinase-3/antagonists & inhibitors , Tissue Inhibitor of Metalloproteinase-3/chemistry , Angiogenesis Inhibitors/chemical synthesis , Animals , Bruch Membrane/injuries , Cells, Cultured , Choroidal Neovascularization/etiology , Choroidal Neovascularization/genetics , Choroidal Neovascularization/metabolism , Endothelium, Vascular , Gene Expression Regulation/drug effects , Humans , Laser Coagulation/adverse effects , Mice , Mice, Inbred C57BL , Peptides/chemical synthesis , Phosphorylation , Signal Transduction/drug effects , Solid-Phase Synthesis Techniques , Tissue Inhibitor of Metalloproteinase-3/genetics , Tissue Inhibitor of Metalloproteinase-3/metabolism , Vascular Endothelial Growth Factor Receptor-1/genetics , Vascular Endothelial Growth Factor Receptor-1/metabolism , Vascular Endothelial Growth Factor Receptor-2/genetics , Vascular Endothelial Growth Factor Receptor-2/metabolism
4.
Am J Pathol ; 180(2): 541-9, 2012 Feb.
Article in English | MEDLINE | ID: mdl-22107828

ABSTRACT

Retention of apolipoprotein B-containing lipoproteins in Bruch's membrane (BrM) is believed to be important in early age-related macular degeneration (AMD). The origin of the lipoproteins in BrM is a hot topic in AMD research. Some studies hypothesize an intraocular origin. BrM is in direct contact to the choriocapillaris; a plasma origin has also been suggested for the low-density lipoprotein (LDL) particles. We developed an animal model to study the biological effects of circulating LDL on the retina. After injection of LDL for 7 days, our results showed evidence of circulating apolipoprotein B100 retention in BrM and showed induction of early AMD-like alterations in the rat retina, such as thickening of BrM, photoreceptor TUNEL-positive cells, and inflammatory cell infiltration. In vitro assays showed that oxidized LDL (ox-LDL) treatment decreased ARPE-19 cell viability in a dose-dependent manner and that 10 mg/L ox-LDL induced marked apoptosis. The ratio of matrix metalloproteinase-2 to tissue inhibitors of metalloproteinase-3 was dysregulated after LDL and ox-LDL treatment in ARPE-19 cells, which can produce profound changes in the extracellular matrix, including thickening of and deposit formation in BrM. The observation that circulating LDL may be a significant, but not complete, origin of the lipoprotein in BrM suggests that these findings can be readily exploited for the development of new model systems and the future benefit of patients with AMD.


Subject(s)
Apolipoprotein B-100/metabolism , Bruch Membrane/drug effects , Capillaries/drug effects , Lipoproteins, LDL/pharmacology , Macular Degeneration/chemically induced , Retinal Pigment Epithelium/drug effects , Animals , Antigens, CD/metabolism , Bruch Membrane/blood supply , Bruch Membrane/ultrastructure , Electroretinography , Immunity, Cellular/physiology , Interleukin-2/metabolism , Lipids/blood , Lipoproteins, LDL/administration & dosage , Male , Matrix Metalloproteinase 2/metabolism , Microscopy, Electron , Rats , Rats, Sprague-Dawley , Retina/metabolism , Retinal Pigment Epithelium/blood supply , Retinal Pigment Epithelium/ultrastructure , Tissue Inhibitor of Metalloproteinase-3/metabolism
5.
FASEB J ; 26(2): 567-75, 2012 Feb.
Article in English | MEDLINE | ID: mdl-22067481

ABSTRACT

Age-related macular degeneration (AMD) is the leading cause of blindness in the Western world. In advanced AMD, new vessels from choriocapillaris (CC) invade through the Bruch's membrane (BrM) into the retina, forming choroidal neovascularization (CNV). BrM, an elastic lamina that is located between the retinal pigment epithelium (RPE) and CC, is thought to act as a physical and functional barrier against CNV. The BrM of patients with early AMD are characterized by decreased levels of antiangiogenic factors, including endostatin, thrombospondin-1 (TSP-1), and pigment epithelium-derived factor (PEDF), as well as by degeneration of the elastic layer. Motivated by a previous report that heat increases elastin expression in human skin, we examined the effect of heat on human ARPE-19 cell production of BrM components. Heat treatment stimulated the production of BrM components, including TSP-1, PEDF, and tropoelastin in vitro and increased the antiangiogenic activity of RPE measured in a mouse corneal pocket assay. The effect of heat on experimental CNV was investigated by pretreating the retina with heat via infrared diode laser prior to the induction of CNV. Heat treatment blocked the development of experimental CNV in vivo. These findings suggest that heat treatment may restore BrM integrity and barrier function against new vessel growth.


Subject(s)
Choroidal Neovascularization/prevention & control , Hot Temperature/therapeutic use , Retinal Pigment Epithelium/blood supply , Angiogenesis Inhibitors/genetics , Angiogenesis Inhibitors/metabolism , Animals , Bruch Membrane/blood supply , Bruch Membrane/metabolism , Bruch Membrane/pathology , Cell Line , Choroidal Neovascularization/genetics , Choroidal Neovascularization/metabolism , Choroidal Neovascularization/pathology , Elastic Tissue/metabolism , Elastic Tissue/pathology , Endostatins/genetics , Endostatins/metabolism , Eye Proteins/genetics , Eye Proteins/metabolism , Gene Expression , Humans , Lasers, Semiconductor/therapeutic use , Macular Degeneration/genetics , Macular Degeneration/metabolism , Macular Degeneration/pathology , Macular Degeneration/therapy , Mice , Mice, Inbred C57BL , Nerve Growth Factors/genetics , Nerve Growth Factors/metabolism , RNA, Messenger/genetics , RNA, Messenger/metabolism , Retinal Pigment Epithelium/metabolism , Retinal Pigment Epithelium/pathology , Serpins/genetics , Serpins/metabolism , Thrombospondin 1/genetics , Thrombospondin 1/metabolism , Tropoelastin/metabolism , Wet Macular Degeneration/genetics , Wet Macular Degeneration/metabolism , Wet Macular Degeneration/pathology , Wet Macular Degeneration/prevention & control
6.
J Cell Physiol ; 225(3): 855-64, 2010 Nov.
Article in English | MEDLINE | ID: mdl-20607799

ABSTRACT

TM601 is a synthetic polypeptide with sequence derived from the venom of the scorpion Leiurus quinquestriatus that has anti-neoplastic activity. It has recently been demonstrated to bind annexin A2 on cultured tumor and vascular endothelial cells and to suppress blood vessel growth on chick chorioallantoic membrane. In this study, we investigated the effects of TM601 in models of ocular neovascularization (NV). When administered by intraocular injection, intravenous injections, or periocular injections, TM601 significantly suppressed the development of choroidal NV at rupture sites in Bruch's membrane. Treatment of established choroidal NV with TM601 caused apoptosis of endothelial cells and regression of the NV. TM601 suppressed ischemia-induced and vascular endothelial growth factor-induced retinal NV and reduced excess vascular permeability induced by vascular endothelial growth factor. Immunostaining with an antibody directed against TM601 showed that after intraocular or periocular injection, TM601 selectively bound to choroidal or retinal NV and co-localized with annexin A2, which is undetectable in normal retinal and choroidal vessels, but is upregulated in endothelial cells participating in choroidal or retinal NV. Intraocular injection of plasminogen or tissue plasminogen activator, which like TM601 bind to annexin A2, also suppressed retinal NV. This study supports the hypothesis that annexin A2 is an important target for treatment of neovascular diseases and suggests that TM601, through its interaction with annexin A2, causes suppression and regression of ocular NV and reduces vascular leakage and thus may provide a new treatment for blinding diseases such as neovascular age-related macular degeneration and diabetic retinopathy.


Subject(s)
Angiogenesis Inhibitors/pharmacology , Annexin A2/metabolism , Bruch Membrane/blood supply , Choroidal Neovascularization/prevention & control , Retinal Neovascularization/prevention & control , Retinal Vessels/drug effects , Retinopathy of Prematurity/prevention & control , Scorpion Venoms/pharmacology , Angiogenesis Inhibitors/administration & dosage , Angiogenesis Inhibitors/metabolism , Animals , Animals, Newborn , Apoptosis/drug effects , Capillary Permeability/drug effects , Choroidal Neovascularization/metabolism , Choroidal Neovascularization/pathology , Choroidal Neovascularization/physiopathology , Disease Models, Animal , Endothelial Cells/drug effects , Endothelial Cells/metabolism , Endothelial Cells/pathology , Female , Fibrinolysin/administration & dosage , Humans , Infant, Newborn , Injections, Intravenous , Mice , Mice, Inbred C57BL , Mice, Transgenic , Promoter Regions, Genetic , Retinal Neovascularization/metabolism , Retinal Neovascularization/pathology , Retinal Neovascularization/physiopathology , Retinal Vessels/metabolism , Retinal Vessels/pathology , Retinal Vessels/physiopathology , Retinopathy of Prematurity/metabolism , Retinopathy of Prematurity/pathology , Retinopathy of Prematurity/physiopathology , Rhodopsin/genetics , Scorpion Venoms/administration & dosage , Scorpion Venoms/metabolism , Tissue Plasminogen Activator/administration & dosage , Vascular Endothelial Growth Factor A/biosynthesis , Vascular Endothelial Growth Factor A/genetics
7.
Microvasc Res ; 80(3): 295-302, 2010 Dec.
Article in English | MEDLINE | ID: mdl-20553963

ABSTRACT

The primary objective of this study was to develop and evaluate new methods of analyzing laser-induced choroidal neovascularization (CNV), in order to make recommendations for improving the reporting of experimental CNV in the literature. Six laser burns of sufficient power to rupture Bruch's membrane were concentrically placed in each eye of 18 adult Norway rats. Eyes received intravitreal injections of either triamcinolone acetonide, ketorolac, or balanced salt solution (BSS). Fluorescein angiography (FA) was performed 2 and 3 weeks after injection, followed by choroidal flat mount preparation. Vascular leakage on FAs and vascular budding on choroidal mounts were quantified by measuring either the cross-sectional area of each CNV lesion contained within the best-fitting polygon using Adobe Photoshop (Lasso Technique or Quick Selection Technique), or the area of bright pixels within a lesion using Image-Pro Plus. On choroidal mounts, the Lasso Technique and Image-Pro Plus detected a significant difference in lesion size between either ketorolac or triamcinolone when compared to BSS, while the Quick Selection Technique did not (Lasso Technique, 0.78 and 0.64; Image-Pro Plus, 0.77 and 0.65). On FA, the Lasso Technique and Quick Selection Technique detected a significant difference in lesion size between either ketorolac or triamcinolone when compared to BSS, while Image-Pro Plus did not (Lasso Tool, 0.81 and 0.54; Quick Selection Tool, 0.76 and 0.57). Choroidal mounts and FA are both valuable for imaging experimental CNV. Adobe Photoshop and Image-Pro Plus are both able to detect subtle differences in CNV lesion size, when images are not manipulated. The combination of choroidal mounts and FA provides a more comprehensive assessment of CNV anatomy and physiology.


Subject(s)
Bruch Membrane/blood supply , Choroidal Neovascularization/pathology , Fluorescein Angiography , Image Interpretation, Computer-Assisted , Lasers, Gas , Microscopy, Fluorescence , Animals , Choroidal Neovascularization/drug therapy , Choroidal Neovascularization/etiology , Cyclooxygenase Inhibitors/administration & dosage , Disease Models, Animal , Glucocorticoids/administration & dosage , Intravitreal Injections , Ketorolac/administration & dosage , Male , Rats , Rats, Inbred BN , Reproducibility of Results , Software , Specimen Handling , Time Factors , Triamcinolone Acetonide/administration & dosage
8.
Am J Pathol ; 168(3): 1031-44, 2006 Mar.
Article in English | MEDLINE | ID: mdl-16507916

ABSTRACT

Vascular repair by adult hematopoietic stem cells (HSCs) is well-appreciated because these cells are known for their plasticity. We have shown that adult HSCs differentiate into endothelial cells and participate in both retinal and choroidal neovascularization. We asked whether HSCs participated in the wounding response by forming astrocytes, retinal pigment epithelia (RPE), macrophages, and pericytes. Lethally irradiated C57BL6/J mice were reconstituted with HSCs from mice homozygous for green fluorescent protein (GFP) and then subjected to laser-induced rupture of Bruch's membrane. After immunohistochemical examination of ocular tissue, GFP(+) astrocytes were observed concentrated along the edge of the laser wound, where they and mural cells closely ensheathed the neovasculature. GFP(+) vascular endothelial cells and macrophages/microglia were also evident. Large irregularly shaped GFP(+) RPE cells constituted approximately 93% of RPE cells adjacent to the edge of the denuded RPE area. In regions farther away from the wound, GFP(+) RPE cells were integrated among the GFP(-) host RPE. Thus, postnatal HSCs can differentiate into cells expressing markers specific to astrocytes, macrophages/microglia, mural cells, or RPE. These studies suggest that HSCs could serve as a therapeutic source for long-term regeneration of injured retina and choroid in diseases such as age-related macular degeneration and retinitis pigmentosa.


Subject(s)
Bruch Membrane/physiology , Choroidal Neovascularization , Hematopoietic Stem Cells/physiology , Pigment Epithelium of Eye/cytology , Retina/cytology , Wound Healing , Animals , Antigens/analysis , Astrocytes/cytology , Bruch Membrane/blood supply , Bruch Membrane/cytology , Bruch Membrane/radiation effects , Cell Differentiation , Green Fluorescent Proteins/analysis , Green Fluorescent Proteins/genetics , Hematopoietic Stem Cells/chemistry , Hematopoietic Stem Cells/cytology , Lasers , Macrophages/chemistry , Macrophages/cytology , Mice , Mice, Transgenic , Microglia/chemistry , Microglia/cytology , Proteoglycans/analysis , Retina/physiology
9.
Invest Ophthalmol Vis Sci ; 45(9): 2886-92, 2004 Sep.
Article in English | MEDLINE | ID: mdl-15326099

ABSTRACT

PURPOSE: To determine the pattern of drusen accumulation with age and to investigate the initial sites of deposition and their relationship to choroidal capillaries in human donor eyes from the eye bank of Moorfields Eye Hospital. METHODS: Wholemounted, hydrated preparations of the choriocapillaris and Bruch's membrane from donor eyes ranging from 42 to 95 years, with or without retinal pigment epithelium (RPE), were examined by conventional and confocal microscopy. Drusen were visualized by their autofluorescence. RESULTS: In all age groups studied autofluorescent drusen were present at the equator but were not found centrally where the vascular architecture is different, being tubular rather than a honeycomb pattern. Autofluorescing drusen were strongly associated with the lateral walls of the choriocapillaris (an area commonly known as the intercapillary pillars of the choriocapillaris (P = 0.028; Wilcoxon signed ranks test). Nonfluorescing drusen were occasionally seen centrally, but were not easily identified, and because of their large size, their localization with respect to capillary walls was not possible. CONCLUSIONS: These results strongly support the notion that autofluorescent drusen are not randomly distributed and have a specific spatial relationship to choroidal vessel walls. That equatorial drusen fluoresce, whereas central drusen do not, suggests that they may have different chemical compositions at the two sites and possibly different significance in age-related macular disease.


Subject(s)
Aging , Choroid/blood supply , Retinal Drusen/pathology , Adult , Aged , Aged, 80 and over , Bruch Membrane/blood supply , Capillaries/pathology , Eye Banks , Fluorescence , Humans , Microscopy, Confocal , Middle Aged , Pigment Epithelium of Eye/pathology , Tissue Donors
10.
Br J Ophthalmol ; 85(1): 40-6, 2001 Jan.
Article in English | MEDLINE | ID: mdl-11133710

ABSTRACT

AIM: To identify if laser photocoagulation induces morphological changes specifically related to the choroidal capillary endothelial processes that protrude into Bruch's membrane. METHODS: Two human eyes and one adult macaque monkey eye received retinal laser photocoagulation that was just suprathreshold, before enucleation or exenteration. They were examined by electron microscopy to determine the length of the endothelial processes emanating from the choroidal capillaries in the region around the laser burn. One human and two monkey untreated eyes were used for comparison. RESULTS: In human eyes, there was no increase in the number of processes 15 hours after laser treatment but at 5 days the processes were more numerous and longer within 400-500 microm of the burn than in the untreated half of the same eye. The processes were longer 9 days after photocoagulation in the monkey, when compared with untreated monkeys, and some breached the elastic lamina, a phenomenon not seen in the untreated eyes. Qualitative differences were also noted in the endothelial cell processes following photocoagulation. Neovascularisation was not observed. CONCLUSIONS: Protrusion of choroidal endothelial cell processes into Bruch's membrane is a normal anatomical feature but the number, length, and morphology of the processes change following mild photocoagulation. It is plausible that these processes may play a part in the clearance of debris from Bruch's membrane, and represent an early stage of angiogenesis. If the latter is true prophylactic laser photocoagulation at just suprathreshold levels may carry a risk of inducing choroidal neovascularisation.


Subject(s)
Choroid/blood supply , Laser Coagulation , Macula Lutea/surgery , Retinal Drusen/prevention & control , Animals , Bruch Membrane/blood supply , Bruch Membrane/ultrastructure , Capillaries/ultrastructure , Endothelium, Vascular/ultrastructure , Female , Fundus Oculi , Humans , Macaca , Microscopy, Electron , Middle Aged
11.
Nat Med ; 5(3): 292-7, 1999 Mar.
Article in English | MEDLINE | ID: mdl-10086384

ABSTRACT

A principal cause of blindness is subretinal neovascularization associated with age-related macular degeneration. Excised neovascular membranes from patients with age-related macular degeneration demonstrated a pattern of Fas+ new vessels in the center of the vascular complex, surrounded by FasL+ retinal pigment epithelial cells. In a murine model, Fas (CD95)-deficient (Ipr) and FasL-defective (gld) mice had a significantly increased incidence of neovascularization compared with normal mice. Furthermore, in gld mice there is massive subretinal neovascularization with uncontrolled growth of vessels. We found that cultured choroidal endothelial cells were induced to undergo apoptosis by retinal pigment epithelial cells through a Fas-FasL interaction. In addition, antibody against Fas prevented vascular tube formation of choroidal endothelial cells derived from the eye in a three-dimensional in vitro assay. Thus, FasL expressed on retinal pigment epithelial cells may control the growth and development of new subretinal vessels that can damage vision.


Subject(s)
Eye/blood supply , Macular Degeneration/physiopathology , Membrane Glycoproteins/biosynthesis , Neovascularization, Pathologic/physiopathology , Retina , Animals , Bone Marrow Cells , Bruch Membrane/blood supply , Capillaries , Endothelium, Vascular/metabolism , Fas Ligand Protein , Humans , Mice , Mice, Inbred C57BL , fas Receptor/biosynthesis
12.
Invest Ophthalmol Vis Sci ; 39(7): 1076-84, 1998 Jun.
Article in English | MEDLINE | ID: mdl-9620066

ABSTRACT

PURPOSE: Because earlier studies indicate that the choroid close to the ora serrata may have unique anatomic features such as wandering cells, blood vessels in Bruch's membrane, and accumulated pigment in the retinal pigment epithelium (RPE), the morphology of the normal human eye at the ora serrata region was investigated. METHODS: Specimens from the ora serrata region of two normal human eyes (male donors, 48 and 52 years old) were investigated by light and electron microscope. Specimens from all quadrants were studied in one eye. RESULTS: The elastic layer of Bruch's membrane extended as far as 15 microm into the peripheral choroid; capillaries were included between the elastin layer and the RPE. Nasally, from the anterior end to 2 mm posterior of the ora serrata, the RPE cells contained more melanin than did those in the adjacent posterior region. Melanin granules in the RPE cells close to the ora either formed large clusters or appeared unusually small because of fragmentation. A unique, fine lamellar, membranous material with a fingerprint-like structure was found between the basal folds of the RPE. This material is also found within the extracellular matrix of the choroid and in association with red blood cells. CONCLUSIONS: The morphology of Bruch's membrane is varied near the ora serrata because capillaries and wandering cells are present in its outer collagenous layer. Unique, fine lamellar, fingerprint-like structures are extruded from the RPE and are removed from the eye together with red blood cells. Capillaries within the inner collagenous region of Bruch's membrane at the ora serrata may not necessarily represent a pathologic response but may be a normal characteristic of thick regions of Bruch's membrane.


Subject(s)
Bruch Membrane/blood supply , Capillaries/ultrastructure , Bruch Membrane/ultrastructure , Eye/blood supply , Humans , Male , Melanins/metabolism , Melanocytes/metabolism , Melanocytes/ultrastructure , Middle Aged , Pigment Epithelium of Eye/ultrastructure
13.
Histol Histopathol ; 7(2): 275-82, 1992 Apr.
Article in English | MEDLINE | ID: mdl-1515711

ABSTRACT

The morphology of the retinal epithelium (RPE), choriocapillaris and Bruch's membrane (complexus basalis) has been investigated by light and electron microscopy in an elasmobranch, the southern fiddler ray or guitarfish (Trygonorhina fasciata). The RPE consists of a single layer of cuboidal cells which display basal (scleral) infoldings as well as numerous apical (vitreal) finger-like processes which interdigitate with the photoreceptor outer segments. The lateral cell borders are relatively smooth and are joined in the mid-region by a series of tight junctions. Internally the RPE nucleus is large, vesicular and centrally located. Smooth endoplasmic reticulum (SER) is abundant while rough endoplasmic reticulum (RER) is scarce. Polysomes are however widespread and mitochondria are plentiful. Two unusual organelles are also noted. One consists of a membrane bound array of tubules while the other is a membrane bound structure consisting of a granular matrix with again an internal tubular array. This species possesses a choroidally located tapetum lucidum in the superior fundus and over this tapetal area, melanosomes are absent from the RPE cells. In non-tapetal locations a few melanosomes are present that do not appear to undergo photomechanical movements. Bruch's membrane is a pentalaminate structure with an almost continuous central elastic layer (lamina densa). The choriocapillaris forms a single layer of capillaries with a thin but only minimally fenestrated endothelium facing Bruch's membrane.


Subject(s)
Fishes/anatomy & histology , Pigment Epithelium of Eye/ultrastructure , Animals , Bruch Membrane/blood supply , Organelles/ultrastructure
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