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At least 793 records · Page 44Linked to original sources
PubMed1999

Histamine immunoreactive axons in the macaque retina.

PURPOSE: The goal of these experiments was to identify the neurotransmitter in centrifugal axons of the macaque retina. METHODS: Macaca mulatta retinas and optic nerves were fixed overnight in carbodiimide and labeled with an antiserum to histamine with the use of an immunofluorescence technique. RESULTS: Several large histamine-immunoreactive axons ran from the optic nerve head to the peripheral retina, where they branched extensively and terminated in the inner plexiform layer, occasionally alongside retinal blood vessels. Other axons that emerged from the optic nerve head ran in the optic fiber layer to the central retina, circled the fovea, and then returned to the optic disc. These may be the source of histamine-immunoreactive axons that have been observed in central visual areas. No labeled cell bodies were present in the retina. Because perikarya in the posterior hypothalamus are the only known source of histamine in the primate central nervous system and because neurons there can be retrogradely labeled from the cut optic nerve, the histamine-immunoreactive axons must have originated there. CONCLUSIONS: Centrifugal axons in the macaque retina are part of the system of axons containing histamine that originate in the hypothalamus and project throughout the brain. Because the activity of these neurons is highest during the morning, histamine might play a role in preparing the retina to operate in daylight. The contacts of histamine-immunoreactive axons with blood vessels suggest that histamine may also play a role in regulating the retinal microvasculature.

Animals↗
PubMed1998

Photoreceptor morphogenesis in the human retina: a scanning electron microscopic study.

There are a number of scanning electron microscopic (SEM) studies on retinal photoreceptors of vertebrates. However, most of these are concerned with the adult retina, and only a very few deal with developing photoreceptors. In man, SEM studies have not been carried out on photoreceptor morphogenesis during fetal or postnatal stages. Hence, the present study was undertaken to examine the sequential morphological changes in developing photoreceptors during different gestational ages in the human retina. Retinas of human fetuses of gestational ages of 10-25 weeks and from autopsy of a 5-month-old infant were processed for SEM. The observations show some new information on the morphogenesis of photoreceptors. At 10-11 weeks, the outer and inner neuroblastic zones are well developed and separated from each other by the layer of Chievitz. By 15-16 weeks, the photoreceptor precursors appear as spherical inner segments on the scleral surface of the outer neuroblastic zone. Cilia develop as small protrusions from the apical ends of the inner segments. Photoreceptor inner segments become arranged in mosaic pattern by 18-19 weeks. In the mosaic, large cone inner segments (putative blue cones) stand out prominently from the remaining small cone inner segments (prospective red/green cones). The rod inner segments are identifiable and show cilia. Between 19-20 and 24-25 weeks, the cone inner segments elongate and change in shape from spherical to oval. At 24-25 weeks, the outer segments develop from the distal ends of rod cilia. At this period, the inner segments of rods and cones are interconnected by protoplasmic projections. Although the precursors of both rods and cones appear to be in a similar state of development at 14-15 weeks gestation, the rods undergo morphological maturation earlier than do the cones. Photoreceptor development in the anterior retina lags behind that of the posterior retina by about 10 weeks. At 5 months after birth, the posterior retina possesses fully developed photoreceptors that are comparable to those of the adult. However, the photoreceptors in the ora serrata resemble those in the posterior retina of 24-25 weeks gestation.

Fetus↗
PubMed1990

The Cohen syndrome: does mottled retina separate a Finnish and a Jewish type?

A new familial cases of the Cohen syndrome in two brothers of one-half second-cousin parents is reported. Typical clinical manifestations of the syndrome; i.e., mental deficiency, hypotonia, characteristic facial appearance, long, narrow hands and feet with elongated fingers, and mottled retinae were present in both patients. Both patients also had leukopenia. Clinical manifestations of the Cohen syndrome in patients are highly variable, and mottled retina has been observed in 22 of 87 patients (25%). However, an association of mottled retina in patients with the Cohen syndrome is likely to be related to the families and ethnic groups. Among 19 familial cases, mottled retina was observed in all affected sibs from five families, but in 13 families none of the affected sibs had the mottled retina. All Finnish patients had the mottled retina, but this was noted in only one of 39 Jewish patients. Based on these data, we hypothesize that two alleles at the gene locus for the Cohen syndrome exhibit different clinical manifestations: one is a Finnish type with mottled retina, and the other is a Jewish type without retinal anomalies.

Abnormalities, Multiple↗
PubMed2004

AII amacrine cells in the mammalian retina show disabled-1 immunoreactivity.

Disabled 1 (Dab1) is an adapter molecule in a signaling pathway, stimulated by Reelin, which controls cell positioning in the developing brain. It has been localized to AII amacrine cells in the mouse and guinea pig retinas. This study was conducted to identify whether Dab1 is commonly localized to AII amacrine cells in the retinas of other mammals. We investigated Dab1-labeled cells in human, rat, rabbit, and cat retinas in detail by immunocytochemistry with antisera against Dab1. Dab1 immunoreactivity was found in certain populations of amacrine cells, with lobular appendages in the outer half of the inner plexiform layer (IPL) and a bushy, smooth dendritic tree in the inner half of the IPL. Double-labeling experiments demonstrated that all Dab1-immunoreactive amacrine cells were immunoreactive to antisera against calretinin or parvalbumin (i.e., other markers for AII amacrine cells in the mammalian retina) and that they made contacts with the axon terminals of the rod bipolar cells in the IPL close to the ganglion cell layer. Furthermore, all Dab1-labeled amacrine cells showed glycine transporter-1 immunoreactivity, indicating that they are glycinergic. The peak density was relatively high in the human and rat retinas, moderate in the cat retina, and low in the rabbit retina. Together, these morphological and histochemical observations clearly indicate that Dab1 is commonly localized to AII amacrine cells and that antiserum against Dab1 is a reliable and specific marker for AII amacrine cells of diverse mammals.

Amacrine Cells↗
PubMed1990

Development redistribution of photoreceptors across the Macaca nemestrina (pigtail macaque) retina.

Redistributions of monkey cones and rods during the first year after birth include a fivefold increase in peak foveal cone density from 43,000 to 210,000 cones/mm2, a decrease in the diameter of the rod-sparse area, and a two- to threefold decrease in peripheral photoreceptor density. Two weeks before birth, higher cone density is already apparent in the future fovea, as are the nasotemporal asymmetry in cone distribution, a higher density "cone streak" along the horizontal meridian, a large rod-sparse central fovea, and a ring of high rod density. Despite the early appearance of these basic patterns, photoreceptor distribution is not mature until 1 to 5 years postnatally. Total cones varied from 4 million at birth to 3.1 million in the average adult. The two oldest eyes had fewer cones, suggesting up to a 25% loss late in development. There were 60 to 70 million rods in the adult macaque retina and little evidence of postnatal changes in number. Neither of these small changes is sufficient to account for the reduction in peripheral photoreceptor density and both are in the wrong direction to explain increasing foveal density, ruling out a major role for either photoreceptor death or generation. Retinal area increased by a factor of 2.4 from 2 weeks before birth to adulthood. In contrast, the posterior pole of the retina was dimensionally stable throughout this period, with the distance between the fovea and optic disc varying nonsystematically from 3.37 to 4.05 mm. Retinal coverage of the globe was also stable at 48-60%. Thus postnatal growth can be ruled out as a factor in the density changes occurring in central retina. Adult retinas have a higher proportion of both cones and rods in midperiphery, whereas young retinas have a higher proportion of photoreceptors in far periphery. It appears that photoreceptors are radially redistributed from peripheral toward central retina during postnatal development, resulting in the marked increase in foveal cone density and the decrease in the eccentricity of the rod ring. Up to 13 weeks postnatally, midperipheral growth of the retina is substantial and increases with eccentricity. At later ages, expansion continues only in the very far periphery. Retinal growth appears sufficient to explain the decreases in peripheral rod and cone density with age. These and previous data strongly suggest that differentiated photoreceptors, with complex cytology and synaptic contacts, migrate toward the foveal center, explaining the increase in foveal photoreceptor density.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

Retinal pathology in Alzheimer's disease. I. Ganglion cell loss in foveal/parafoveal retina.

Morphometric analysis of the numbers of neurons in the ganglion cell layer (GCL) of the central retina (fovea/foveola/parafoveal retina) in eyes from 9 Alzheimer's disease (AD) and 11 age-matched control cases revealed an overall decrease of 25% in total numbers of neurons in AD as compared with control eyes. Detailed analyses of GCL neurons at various eccentricities from the foveola showed that the greatest decrease in neuronal density (43% decrease) occurred in the central 0-0.5 mm (foveal region), while at 0.5-1 mm and at 1-1.5 mm eccentricities, neuronal loss amounted to 24 and 26%, respectively. The temporal region of the central retina appeared most severely affected, with up to 52% decrease in neuronal density near the foveola (central 0-0.5 mm eccentricity). There was close agreement between fellow eyes analyzed separately for three AD and three control cases. Analysis of neuronal sizes showed that all sizes of neurons were similarly affected in AD. In the GCL of control retinas, neurons decreased with age (coefficient of correlation = -0.67), while in AD retinas no such relationship was evident. Since in the central 0-2 mm region of the retina 97% of neurons in the GCL are ganglion cells (while the remaining 3% consist of displaced amacrine cells), these results demonstrate extensive ganglion cell loss in the central retina in AD.

Age Distribution↗
PubMed1995

The persistence of cone photoreceptors within the dorsal retina of aged retinally degenerate mice (rd/rd): implications for circadian organization.

Rod- and cone-opsin specific antibodies were used in an attempt to immunolabel remaining photoreceptor cells in the mutant rd (retinal degeneration) mouse retina. We identified a region-specific distribution in the pattern of photoreceptor degeneration, with the dorsal retina showing markedly less photoreceptor degeneration than the ventral retina. All rod and cone immunoreactive cells disappeared in the ventral retina by 100-120 days of age. By contrast, both cone and a small number of rod immunopositive cells were identified in the dorsal retina at this time. By 200 days all rod immunoreactive cells had disappeared. At 360 days numerous cone immunoreactive cells remained within a restricted region of the dorsal retina. As rd mice show unattenuated circadian responses to light, these remaining photoreceptor cells within the dorsal retina become candidates for the regulation of circadian physiology by light.

Age Factors↗
PubMed2005

Up-regulated expression of neuronal nitric oxide synthase in experimental diabetic retina.

Nitric oxide (NO) can play either a neuroprotective or a neurotoxic role in diverse neurodegenerative conditions. This study investigated the differential expression of neuronal nitric oxide synthase (nNOS) in the streptozotocin-induced diabetic rat retina to clarify the involvement of NO produced from neurons in the early pathogenesis of diabetic retinopathy. A decrease in thickness of the outer retina was evident at 12 and 24 weeks after onset of diabetes. nNOS was immunolocalized in two subtypes of amacrine cells, displaced amacrine cells and in some bipolar cells in the normal retinas. The densities of each type of nNOS-expressing neuron showed no significant differences in the diabetic retinas with the exception of the bipolar cells. The numbers of nNOS bipolar cells at 12 weeks of diabetes increased threefold, showing dendritic polarity of nNOS expression. Protein levels of nNOS increased throughout the diabetic retinas reaching a peak value at 24 weeks of diabetes. Thus, diabetes up-regulates the expression of nNOS in bipolar cells, and NO from these cells may aggravate the degeneration of the outer retina in the diabetic retinas.

Amacrine Cells↗
PubMed1989

Clonal origins of cells in the pigmented retina of the zebrafish eye.

Mosaic analysis has been used to study the clonal basis of the development of the pigmented retina of the zebrafish, Brachydanio rerio. Zebrafish embryos heterozygous for a recessive mutation at the gol-1 locus were exposed to gamma-irradiation at various developmental stages to create mosaic individuals consisting of wild-type pigmented cells and a clone of pigmentless (golden) cells in the eye. The contribution of individual embryonic cells to the pigmented retina was measured and the total number of cells in the embryo that contributed descendants to this tissue was determined. Until the 32-cell stage, almost every blastomere has some descendants that participate in the formation of the pigmented retina of the zebrafish. During subsequent cell divisions, up to the several thousand-cell stage, the number of ancestral cells is constant: approximately 40 cells are present that will give rise to progeny in the pigmented retina. Analysis of the size of clones in the pigmented retina indicates that the cells of this tissue do not arise through a rigid series of cell divisions originating in the early embryo. The findings that each cleavage stage cell contributes to the pigmented retina and yet the contribution of such cells is highly variable are consistent with the interpretation that clonal descendants of different blastomeres normally intermix extensively prior to formation of the pigmented retina.

Animals↗
PubMed1995

Isoprenoid lipid metabolism in the retina: dynamics of squalene and cholesterol incorporation and turnover in frog rod outer segment membranes.

Frogs were injected intravitreally with [3H]acetate, and the formation of [3H]-labeled squalene and cholesterol in the retina and their incorporation into rod outer segment (ROS) membranes were evaluated biochemically over a 60-day time course. ROS [3H]squalene specific activity was maximal by 1-3 days, then declined with a half-time of approximately 20-30 days. In contrast, the specific activity of ROS [3H]cholesterol initially increased to a level substantially less than that of [3H]squalene, and then remained constant. Thus, ROS squalene appears to turn over without obligatory conversion to, or coturnover with, ROS cholesterol. When [3H]acetate was injected into one eye, radiolabel in non-saponifiable lipids of the contralateral retina represented < 1% of those recovered from the ipsilateral retina; hence, systemic contributions to de novo synthesis were obviated. Long-term (> or = 8 hr) in vitro incubations of isolated retinas with [3H]acetate resulted in incorporation of [3H]-labeled sterols and squalene into ROS, at levels comparable to those observed in ROS from companion incubated eyecup preparations and from retinas 8 hr after intravitreal injection of [3H]acetate. These results demonstrate that the in vitro system faithfully reflects the in vivo biosynthetic capacity with respect to isoprenoid lipid metabolism, and suggest that de novo synthesis within the neural retina is responsible for generating most, if not all, of the [3H]squalene and [3H]cholesterol formed under the given conditions. Treatment of retinas in vitro with brefeldin A or energy poisons blocked transport of newly synthesized opsin, but not squalene, to the ROS. Furthermore, frogs maintained at 8 degrees C exhibited marked suppression of incorporation of newly synthesized protein into the ROS, while [3H]squalene incorporation was only minimally reduced, compared with frogs maintained at 22 degrees C. These results are consistent with prior findings that suggest that lipids are transported to the ROS by a mechanism distinct and independent from that employed for intracellular trafficking of opsin and other ROS-destined membrane proteins.

Animals↗
PubMed1987

Endocytosis in the inner segment of rod photoreceptors: analysis of Xenopus laevis retinas using horseradish peroxidase.

To evaluate endocytosis in rod photoreceptor inner segments, isolated retinas from Xenopus laevis were maintained in vitro in the presence of the tracer, horseradish peroxidase (HRP). HRP-positive vesicles, 110 +/- 82 nm in diam. (mean +/- S.D.), appeared in the inner segment cytoplasm within 2 min of incubation. Within 8-15 min, 20-30% of the vesicles in the ellipsoid were HRP-positive, reaching approx. 50% by 30-60 min and maintaining this level through 4 hr of culture. In retinas incubated 30 min with HRP and then cultured for an additional period without tracer, the HRP-labeled vesicles were reduced in number by 50- and 75% in the 1- and 2-hr chase incubations, respectively. In retinas cultured for 8 min or longer, multivesicular bodies in the inner segments also contained HRP reaction product, suggesting that the HRP-labeled endocytotic vesicles enter multivesicular bodies. Retinas cultured with HRP for greater than or equal to 1 hr contained significantly more vesicles (per unit area of ellipsoid cytoplasm) as compared with unincubated retinas, retinas incubated from 1 hr in normal media or retinas incubated 30 min with HRP followed by normal chase medium for greater than or equal to 30 min. Taken together, these data indicate that the rod photoreceptor inner segment is capable of extensive endocytotic activity, a process which may function to recover components of the inner segment plasma membrane and the interphotoreceptor matrix.

Animals↗
PubMed2002

Partial re-incorporation of corner cones in the retina of the Atlantic salmon (Salmo salar).

The distribution of corner (putative ultraviolet-sensitive) cones in the retina of Atlantic salmon was examined from the small juvenile (parr) stage to the adult stage (approaching sexual maturation). Small parr weighing approximately 5 g lacked corner cones everywhere except, mainly, near the dorsal periphery. Large fish ( approximately 5 kg) approaching sexual maturation showed corner cones in other areas of the dorsal retina besides the periphery. These areas, characterized by low resolving power, had similar corner cone densities to analogous areas in the smolt retina, suggesting that corner cones are formed in the periphery and incorporated into the dorsal retina of the Atlantic salmon sometime during the smolt stage. This incorporation is partial both in numbers of cones and in location (only the dorsal retina is affected). These findings contrast with the situation in rainbow trout where corner cones from existing mosaics are only partially lost from the ventral retina, if at all, and where production and incorporation of these cones into the dorsal retina occurs throughout life. Thus, in salmonids, there are at least two different strategies that determine retinal corner cone distributions.

Aging↗
PubMed2002

Expression of p75(NTR) in photoreceptor cells of dystrophic rat retinas.

Although a gene mutation in the Royal College of Surgeons (RCS) dystrophic rat results in defective phagocytosis and in accumulation of debris in the subretinal space, the molecular mechanisms leading to photoreceptor cell death remain unclear. In this study, the expression of p75(NTR), the low-affinity neurotrophin receptor incriminated in the apoptosis of developing neurons, was investigated at various stages of retinal degeneration in dystrophic rats using immunohistochemistry, in situ reverse transcription polymerase chain reaction (RT-PCR), Western blot, and relative RT-PCR. In normal adult retinas, p75(NTR) immunolabeling was observed mainly in the outer limiting membrane, with punctate labeling in the inner nuclear and ganglion cell layers. In 18- to 30-day-old dystrophic retinas, the immunostaining appeared to increase especially in the photoreceptor outer and inner segments. Dense staining was also observed in the retinal pigment epithelium (RPE) and choroid. In 60-day-old dystrophic rat retinas, the density of immunolabeling for p75(NTR) increased dramatically in the remaining inner retina, especially in the inner nuclear, inner plexiform, and ganglion cell layers. Post-embedding immunogold labeling of normal retinas verified the distribution of p75(NTR) in photoreceptor cells within the inner segments, cell bodies, and outer segments. The apparent increased intensity in p75(NTR) immunostaining in dystrophic retinas was verified by Western blots and densitometric analyses. In situ RT-PCR and relative RT-PCR further established increased synthesis of p75(NTR) in dystrophic retinas. The increased levels of p75(NTR) in the RPE and photoreceptor cells, the initial sites of injury, during retinal degeneration in dystrophic rats strongly suggest that altered expression of p75(NTR) may be directly involved in photoreceptor death.

Animals↗
PubMed1999

Basement membrane and growth factor gene expression in normal and diabetic human retinas.

PURPOSE: Recently, we found abnormal accumulation of several extracellular matrix components in retinal basement membranes in human diabetic retinopathy (DR). Others have described increased levels of various growth factors within the vitreous of DR patients. This study examined mRNA levels of these extracellular matrix components and growth factors within human retinal tissues. METHODS: Total retinal RNA was analyzed by semiquantitative reverse transcription-polymerase chain reaction (RT-PCR). RT-PCR products were identified by Southern blotting. Samples were normalized with respect to beta2-microglobulin cDNA. Twenty-one retinas were analyzed: 6 normal, 7 diabetic without DR and 8 diabetic with DR. RESULTS: In diabetic retinas without DR, the expression levels of most genes were similar to normal. In DR retinas, tenascin-C mRNA expression increased compared to both normal and diabetics without DR. By RT-PCR and Northern blotting, mainly small tenascin-C mRNA isoforms were expressed, and some of them were elevated in DR retinas. Fibronectin mRNA was elevated in DR compared to normal retinas, possibly due to the overexpression of extradomain A-containing isoform (ED-A+, or cellular fibronectin). In DR retinas, gene expression of vascular endothelial growth factor and placenta growth factor was elevated compared to normal, although mRNA for these growth factors receptors (VEGFR-1/Flt-1 and VEGFR-2/KDR) did not change significantly. Transforming growth factor-beta1 mRNA also increased in DR retinas. CONCLUSIONS: The data suggest that proliferative DR development may be associated with increased retinal expression of vascular endothelial growth factor, placenta growth factor and transforming growth factor-beta1 that possibly triggers the deposition of small tenascin-C isoforms in the blood vessel walls. Angiogenesis-stimulating tenascin-C may further promote diabetic retinal neovascularization.

Aged↗
PubMed2004

Identification of ON-OFF direction-selective ganglion cells in the mouse retina.

We identified the ON-OFF direction-selective ganglion cells (DSGCs) in the mouse retina and characterized their physiological, morphological and pharmacological properties. These cells showed transient responses to the onset and termination of a stationary flashing spot, and strong directional selectivity to a moving rectangle. Application of various pharmacological reagents demonstrated that the ON-OFF DSGCs in the mouse retina utilize a similar array of transmitters and receptors to compute motion direction to their counterparts in the rabbit retina. Voltage clamp recording showed that ON-OFF DSGCs in the mouse retina receive a larger inhibitory input when the stimulus is moving in the null direction and a larger excitatory input when the stimulus is moving in the preferred direction. Finally, intracellular infusion of neurobiotin revealed a bistratified dendritic field with recursive dendrites forming loop-like structures, previously classified as RG(D2) by morphology. Overall, the ON-OFF DSGCs in the mouse retina exhibit almost identical properties to their counterparts in the rabbit retina, indicating that the mechanisms for computing motion direction are conserved from mouse to rabbit, and probably also to higher mammals. This first detailed characterization of ON-OFF DSGCs in the mouse retina provides fundamental information for further study of maturation and regulation of the neuronal circuitry underlying computation of direction.

Action Potentials↗
PubMed2004

Angiopoietin-2 causes pericyte dropout in the normal retina: evidence for involvement in diabetic retinopathy.

Pericyte loss is an early pathologic feature of diabetic retinopathy, consistently present in retinae of diabetic humans and animals. Because pericyte recruitment and endothelial cell survival are controlled, in part, by the angiopoietin/Tie2 ligand/receptor system, we studied the expression of angiopoietin-2 and -1 in relation to the evolution of pericyte loss in diabetic rat retinae, using quantitative retinal morphometry, and in retinae from mice with heterozygous angiopoietin deficiency (Ang-2 LacZ knock-in mice). Finally, recombinant angiopoietin-2 was injected into eyes of nondiabetic rats, and pericyte numbers were quantitated in retinal capillaries. Angiopoietin-1 protein was present in the normal maturing retina and was upregulated 2.5-fold in diabetic retinae over 3 months of diabetes. In contrast, angiopoietin-2 protein was consistently upregulated more than 30-fold in the retinae of diabetic rats, preceding the onset of pericyte loss. Heterozygous angiopoietin-2 deficiency completely prevented diabetes-induced pericyte loss and reduced the number of acellular capillary segments. Injection of angiopoietin-2 into the eyes of normal rats induced a dose-dependent pericyte loss. These data show that upregulation of angiopoietin-2 plays a critical role in the loss of pericytes in the diabetic retina.

Angiopoietin-1↗
PubMed2005

Neutrophils are associated with capillary closure in spontaneously diabetic monkey retinas.

Type 2 diabetes develops spontaneously in obese aging rhesus monkeys (Macaca mulatta). This study investigates the association between polymorphonuclear leukocytes and development of retinopathy. Blood pressure and plasma glucose levels were determined in 15 diabetic and 6 nondiabetic monkeys. The plasma levels of total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides were determined just before the start of the animal's final decline and elective necropsy. Retinas were incubated for ADPase (labels viable retinal blood vessels) and nonspecific esterase (labels neutrophils) activities. Polymorphonuclear leukocytes were counted per millimeter squared of retina. After the retina was flat-embedded in glycol methacrylate, tissue sections were taken through areas of interest and observed microscopically. Elevated numbers of intravascular polymorphonuclear leukocytes were present adjacent to areas with retinal capillary nonperfusion. There were significantly more polymorphonuclear leukocytes per millimeter squared in diabetic retinas (6.91 +/- 5.01) compared with normal retinas (1.45 +/- 1.62, P = 0.018). Severity of hypertension in diabetes was also significantly associated with greater numbers of polymorphonuclear leukocytes (P = 0.02). There was a significant positive exponential correlation between the number of polymorphonuclear leukocytes per millimeter squared and the level of total cholesterol (R = 0.907), LDL cholesterol (R = 0.875), the total cholesterol-to-HDL cholesterol ratio (R = 0.86), and total triglycerides (R = 0.888). This study demonstrates that severity of diabetes and the development of retinopathy are associated with increased numbers of polymorphonuclear leukocytes in the retina of diabetic monkeys. Hypertension, high plasma levels of LDL cholesterol and triglycerides, and low plasma levels of HDL cholesterol also are associated with increased polymorphonuclear leukocytes in retina.

Aneurysm↗
PubMed2002

Altered expression patterns of VEGF receptors in human diabetic retina and in experimental VEGF-induced retinopathy in monkey.

PURPOSE: The vascular endothelial growth factor (VEGF) family is involved in vascular leakage and angiogenesis in diabetic retinopathy (DR) in the eye, but may also have physiological functions. Based on the hypothesis that differential VEGF receptor (VEGFR) expression in the retina is an important determinant of effects of VEGF, this study was conducted to investigate VEGFR expression in the diabetic retina and in an experimental monkey model of VEGF-A-induced retinopathy. METHODS: In retinas of 27 eyes of diabetic donors, 18 eyes of nondiabetic control donors, and 4 monkey eyes injected with PBS or VEGF-A, expression patterns of VEGFR-1, -2, and -3 in relation to leaky microvessels, as identified by the marker pathologische anatomie Leiden-endothelium (PAL-E) were studied by immunohistochemistry. RESULTS. In control human retinas and retinas of PBS-injected monkey eyes, all three VEGFRs were expressed in nonvascular areas, but only VEGFR-1 was constitutively expressed in retinal microvessels. In diabetic eyes, increased microvascular VEGFR-2 expression was found in association with PAL-E expression, whereas microvascular VEGFR-3 was present in a subset of PAL-E-positive cases. In VEGF-A-injected monkey eyes, VEGFR-1, -2, and -3 and PAL-E were expressed in retinal microvessels. CONCLUSIONS: The VEGFR-1, -2, and -3 expression patterns in control retinas suggest physiological functions of VEGFs that do not involve the vasculature. Initial vascular VEGF signaling may act primarily through VEGFR-1. In diabetic eyes, expression of retinal VEGFR-2 and -3 is increased, mainly in leaky microvessels, and VEGF-A induces vascular expression of the VEGF-A receptor VEGFR-2 and the VEGF-C/D receptor VEGFR-3. These findings indicate a dual role of VEGFs in the physiology and pathophysiology of the retina and suggest that microvascular VEGFR-2 and -3 signaling by VEGFs occurs late in the pathogenesis of DR, possibly initiated by high levels of VEGF-A in established nonproliferative DR.

Aged↗