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Results for “retinal microvascular”

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At least 19 recordsLinked to original sources

PubMed1991

Effect of varying oxygen concentrations on the proliferation of retinal microvascular cells in vitro.

Microvascular fragments and pure cultures of either retinal microvascular endothelial cells, retinal pericytes or Tenon's capsule fibroblasts were grown on a gas permeable substrate while exposed to varying oxygen concentrations (5, 10, 20, 40 and 95% oxygen). For all three cell types cell proliferation was greatest under the lowest oxygen concentration and decreased as the oxygen concentration increased. The decrease in the proliferative ability of cells exposed to the higher oxygen concentrations could be reversed if the cells were returned to a normoxic environment. Endothelial cells were the most sensitive to changes in oxygen tensions showing a proliferative response after 24 hr exposure as opposed to 48 hr for pericytes and fibroblasts. These results suggest a direct mechanism by which the intra-vitreal and intra-retinal oxygen tension may influence both the development of preretinal new vessels (in response to retinal ischaemia) and also the regression of neovascularization following scatter photocoagulation or vitrectomy.

Animals↗

PubMed1992

Inhibition of bovine retinal microvascular pericyte proliferation in vitro by adenosine.

Adenosine acts on bovine retinal microvascular pericytes through one or more adenosine receptor subtypes present on the cell surface. Retinal pericytes cultured in medium containing adenosine at concentrations from 10(-6) to 10(-4) M showed significant reduction in proliferation following several days in vitro compared with control cultures. The effects of adenosine were mimicked by polyadenylic acid and inhibited by 8-phenyltheophylline, indicating involvement of a cell surface receptor. Metabolites of adenosine had no effect on pericyte proliferation. An A2 adenosine receptor-specific analogue also inhibited pericyte growth, suggesting that inhibition by adenosine is mediated by A2-receptors and might involve a transient increase in adenosine 3',5'-cyclic monophosphate levels. The results of the present study demonstrate that in addition to demonstrated stimulatory effects on capillary endothelial cells, adenosine also has a direct inhibitory effect on retinal pericytes. We hypothesize a dual function of adenosine within the capillary wall resulting in loss of inhibition of endothelial cells and suggest a role for this nucleoside in pathological neovascularization processes such as proliferative diabetic retinopathy.

Adenosine↗

PubMed1991

Human growth hormone stimulates proliferation of human retinal microvascular endothelial cells in vitro.

Growth hormone (GH) has been implicated in the pathogenesis of proliferative diabetic retinopathy. We sought to determine whether this could be mediated by an effect of GH on proliferation of endothelial cells, and, for this purpose, established long-term cultures of human retinal microvascular endothelial cells (hREC) from normal postmortem human eyes. High-purity (greater than 95%) hREC preparations were selected for experiments, based on immunofluorescence with acetylated low density lipoprotein (LDL) and anti-factor VIII-related antigen. Growth requirements for these cells were complex, including serum for maintenance at slow growth rates and additional mitogens for more rapid proliferation. Exposure of hREC to physiologic doses of human GH (hGH) resulted in 100% greater cell number vs. control (P less than 0.01) but could be elicited only in the presence of serum. When differing serum conditions were compared, hGH stimulated [3H]thymidine incorporation up to 1.6- to 2.2-fold under each condition and increased DNA content significantly in the presence of human, horse, and fetal calf serum. Depending on the culture conditions used, the threshold hGH concentration for significant stimulation of hREC proliferation was 0.4-4 micrograms/liter. In contrast, proliferation of human umbilical vein endothelial cells was not significantly altered by hGH added to concentrations as high as 200 micrograms/liter. In summary, hREC respond to physiologic concentrations of hGH in vitro with enhanced proliferation. This specific effect of GH on retinal microvascular endothelial cells supports the hypothesis of a role for GH in endothelial cell biology.

Cell Division↗

PubMed1992

The effect of endothelin 1 on the retinal microvascular pericyte.

The effect of the highly vasoactive peptide endothelin 1 (ET1) was tested on bovine retinal microvascular pericytes propagated in vitro. Specific binding of 125I-ET1 to retinal pericytes was documented by autoradiography. ET1 caused contraction of pericytes at a concentration of 0.1 nM which was accompanied by increases in inositol phosphates. Exposure of pericytes to 10 nM ET1 resulted in the aggregation and realignment of muscle-specific actins into bundles which were oriented parallel to the long axis of the cell, and ET1 was also mitogenic to pericytes in the presence of low levels of fetal calf serum. These observations suggest that ET1 may play an important role in endothelial cell-pericyte interactions within the microvasculature of the retina and that it may be involved in the autoregulation of retinal blood flow.

Actins↗

PubMed1992

Effects of cholinergic and adrenergic agonists on adenylate cyclase activity of retinal microvascular pericytes in culture.

Pericytes are contractile cells that might help regulate microvascular blood flow. To understand their potential role in the regulatory responses of the retina and optic nerve head vessels, the response of pericytes isolated from bovine retinal microvessels was determined to oxotremorine, isoproterenol, phenylephrine, and clonidine. Isoproterenol doubled the basal levels of cyclic adenosine monophosphate (cAMP) specifically through beta-adrenergic receptors, because the effect was blocked by dl-propranolol. The alpha 1 agonist phenylephrine did not induce any major change in adenylate cyclase activity. The alpha 2 agonist clonidine decreased basal cAMP synthesis and reduced the effect of isoproterenol. The cholinergic agonist oxotremorine did not modify the basal activity of adenylate cyclase but was able to decrease by almost 50% the forskolin-induced increase of cAMP. These results suggest that pericytes have functional adrenergic and cholinergic receptors, and they might respond to autonomic vasoactive substances present in vivo.

Adenylyl Cyclases↗

PubMed1990

Phosphoinositide metabolism and prostacyclin formation in retinal microvascular endothelium: stimulation by adenine nucleotides.

Phosphoinositide lipid metabolism and prostacyclin production are implicated in endothelium dependent vascular relaxation in large blood vessels. To determine if these biochemical pathways might be involved in the regulation of microvascular tone in the retina, we measured the formation of 6-keto-prostaglandin-F1 alpha, the stable end product of prostacyclin, and inositol phosphates from 3H-labeled phosphoinositide lipids, in endothelial cells prepared from bovine retinal microvessels and maintained in long-term culture. We found that adenosine 5'-triphosphate and adenosine 5'-diphosphate both stimulated a dose-dependent accumulation of inositol phosphates and of 6-keto-prostaglandin-F1 alpha in these cells. The agonist specificity of the responses, with stimulation by adenosine 5'-triphosphate and adenosine 5'-diphosphate, and inactivity of adenosine 5'-monophosphate and adenosine, suggest that they are mediated through P2 purinergic receptors. The similar early time courses of 6-keto-prostaglandin-F1 alpha and inositol triphosphate production support the hypothesis that prostacyclin formation could result from the mobilization of intracellular calcium by inositol triphosphate, which activates phospholipase A, and thereby releases arachidonic acid to form prostacyclin. These findings point to a role for these cells in the regulation of normal retinal vascular tone. Because phosphoinositide lipid metabolism is altered in diabetes, dysfunction of these biochemical pathways in retinal endothelium could underlie the pathophysiology of diabetic retinopathy.

6-Ketoprostaglandin F1 alpha↗

PubMed1987

Ultrastructural studies of bovine retinal microvascular basement membranes with the cationic dye ruthenium red.

Our recent observation that the basement membranes of brain microvessels do not stain with the cationic dye ruthenium red has raised the question of whether the basement membranes of this and other vascular beds functioning as barriers between blood and neural tissues are deficient in the polyanionic macromolecules, such as glycosaminoglycans, which are responsible for the ruthenium red staining of other vascular basement membranes. We therefore attempted to produce staining in the only barrier-type microvascular basement membrane known to contain heparan sulfate. Bovine retinas were fixed by immersion in aldehyde fixatives containing ruthenium red, buffered with either 10 mM or 100 mM sodium cacodylate. We found discrete, electron-dense deposits of ruthenium red in vascular basement membranes, quite similar to those seen in vascular basement membranes of nonneural tissues after exposure to ruthenium red. These deposits were more distinct and more frequent in tissue exposed to ruthenium red-aldehyde solutions buffered with 10 mM cacodylate. They were not seen if ruthenium red was omitted from the fixative. The results demonstrate that anionic macromolecules in basement membranes of barrier-type microvessels can be stained with cationic dyes, and suggest that the failure of brain microvessels to stain with ruthenium red may be the result of a relative or total lack of polyanion in this basement membrane, or of other unique properties.

Animals↗

PubMed1992

Preparation of fluorescent basic fibroblast growth factor: localization in living retinal microvascular endothelial cells.

A biologically active fluorescent derivative of recombinant human basic fibroblast growth factor (bFGF) was prepared by immobilization on heparin-Sepharose 4B (HS) and derivatization with the fluorophore, Texas Red (TR). TR-bFGF was separated from free dye and carrier protein by elution from HS using 1.5 M NaCl. TR-bFGF contained an average of two dye molecules bound per bFGF, retained its mitogenic activity and was visible using a fluorescence microscope equipped with silicon intensified target camera (SIT). TR-bFGF stimulated the growth of bovine aortic endothelial cells (BAEC), microvessel endothelial cells (MVEC) and BHK-21 cells grown in culture. BAEC, MVEC and BHK-21 cells treated with 20 ng ml-1 (1 nM) TR-bFGF for 72 hr were stimulated over serum controls by 87, 26 and 6%, respectively. TR-bFGF stimulated EC growth was inhibited in a dose-dependent fashion when cells were coincubated with microM chloroquine. When EC were treated with TR-bFGF at 4 degrees C and then monitored at 37 degrees C, bright, focal, cytoplasmic spots were observed, which accumulated as punctate, perinuclear fluorescence. EC internalization of TR-bFGF was inhibited 80% by the addition of 100-fold molar excess unlabeled bFGF or by maintaining cultures at 4 degrees C. TR-bFGF colocalized with an EC lysosomal marker, but TR-bFGF was not detected in the nucleus. Results of these localization studies suggest that TR-bFGF stimulates EC proliferation without entering the nucleus.

Cell Division↗

PubMed2026

Effect of Bariatric Surgery on Improvement of Retinal Microvasculature in Patients With Obesity: A Systematic Review and Meta-Analysis.

Obesity is associated with adverse retinal microvascular changes, including narrower central retinal arteriolar equivalent (CRAE), wider central retinal venular equivalent (CRVE) and lower arteriovenous ratio (AVR). Although bariatric surgery improves cardiometabolic risk, its effect on retinal microvascular calibre remains uncertain. We systematically searched the Cochrane Library, PubMed, ScienceDirect and Scopus up to June 2026. Prospective cohort studies reporting CRAE, CRVE or AVR before and after bariatric surgery in patients with obesity were included. Risk of bias was assessed using the Newcastle-Ottawa Scale. Pooled mean differences (MD) with 95% confidence intervals (CI) were calculated using a random-effects model. Eight prospective cohort studies including 283 patients were included. Seven studies contributed to the CRAE and CRVE analyses, and seven contributed to the AVR analysis. Bariatric surgery was associated with a significant increase in CRAE (MD = +4.02 μm, CI [0.26-7.78], p = 0.04). Sensitivity analysis excluding one study showed a stronger and more consistent effect (MD = +5.41 μm, CI [4.59-6.22], p < 0.01). CRVE significantly decreased after surgery (MD = -6.75 μm, CI [-7.42 to -6.07], p < 0.01), while AVR significantly increased (MD = +0.03, CI [0.02-0.05], p < 0.01). Sensitivity analyses suggested that the direction of effect was generally robust, although between-study heterogeneity was present. Bariatric surgery may be associated with favourable retinal microvascular changes in patients with obesity, reflected by increased CRAE and AVR and decreased CRVE.

Humans↗

PubMed1990

Inhibition of microvascular endothelial cell proliferation by vitreous following retinal scatter photocoagulation.

Laser photocoagulation of pig retina induced breakdown of the blood-retinal barrier, with the appearance of serum proteins in the vitreous as determined by sodium dodecyl sulphate/polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting techniques. Vitreous from lasered eyes inhibited the proliferation of cultured retinal microvascular endothelial cells in comparison with vitreous from non-lasered control eyes, and the inhibitory effect in the lasered eyes persisted for at least seven days. Inhibition was specific for endothelial cells, since no effect was observed when retinal pericytes or Tenon's fibroblasts were the target cells. These results suggest that indirect scatter photocoagulation may induce regression of neovascularisation by causing breakdown of the blood-retinal barrier and thus releasing into the vitreous serum components which result in inhibition of retinal microvascular endothelial cell growth.

Animals↗

PubMed1992

Biological activities of vitreous gel, retrohyaloid fluid and subretinal fluid from diabetic and non-diabetic eyes.

This study compared the effects of vitreous gel, retrohyaloid fluid and subretinal fluid from diabetic and non-diabetic eyes on the proliferation and migration of retinal microvascular cells in vitro. Intraocular fluids were obtained from eyes undergoing repair of retinal detachment, due either to proliferative diabetic retinopathy or rhegmatogenous retinal detachment associated with a degree of proliferative vitreoretinopathy. The results demonstrated that the intraocular stimulatory activity for the proliferation of retinal microvascular endothelial cells varied between the different ocular compartments. The mitogenic and migrational activity in vitreous gel was greater than that of either the subretinal or retrohyaloid fluids of the same eye, and the activity of subretinal fluid was intermediate between that of the vitreous gel and the retrohyaloid fluid. There was no significant difference between the activities of the samples from diabetic and non-diabetic eyes.

Body Fluids↗

PubMed1991

Microvascular endothelial-derived autacoids regulate pericyte contractility.

A silicone rubber assay is used in conjunction with morphometric measurements to characterize in vitro the contractile properties of retinal pericytes in response to endothelial secreted factors. Factor(s) present in conditioned media derived from pulmonary and retinal microvascular endothelial cells and pulmonary artery endothelial cells promote pericyte contractions. Using a radioimmunoassay significant levels of endothelin immunoreactivity are measured in conditioned media obtained from all three cell lines. Thrombin treatment enhanced endothelin-like secretions by pulmonary microvascular endothelial cells, but significantly reduced levels of endothelin-like immunoreactivity secreted by retinal microvascular endothelial cells. Synthetic endothelin and thromboxane A2 (TxA2) stimulate pericyte contractions, whereas prostaglandin I2 (PGI2) promotes pericyte relaxation. Thrombin and angiotension II (ang II) have no effect on pericyte contractility. However, using cocultures of pericytes and endothelial cells we observe endothelial-dependent pericyte contractions in response to thrombin and ang II. Thrombin and ang II stimulate the release of endothelial-derived contracting factors, with characteristics similar to endothelin. These data suggest microvascular endothelial cell-pericyte interactions may regulate, at least in part, microvessel contractility.

Angiotensin II↗

PubMed1992

Steroid inhibition of neural microvessel morphogenesis in vitro: receptor mediation and astroglial dependence.

Steroid hormones alter several aspects of microvascular function within the CNS. Both microvessel formation and blood-brain barrier expression appear to be influenced by interactions between astrocytes and endothelial cells. To determine if steroids alter astrocyte-endothelial interactions, we studied their effects on astroglial-induced microvessel morphogenesis in vitro. C6 astroglial cells induce bovine retinal microvascular endothelial cells to differentiate into capillary-like structures. Dexamethasone, hydrocortisone, and progesterone at 10 nM inhibited C6-induced microvessel morphogenesis by 75, 35, and 30%, respectively. Inhibition by dexamethasone was both time and concentration dependent, reaching 80-100% at 1 microM. Tetrahydrocortisone and 17 alpha-hydroxyprogesterone had only marginal inhibitory effects. Cortexolone, a glucocorticoid receptor antagonist, blocked inhibition by dexamethasone. Progesterone receptors were expressed in C6 but not bovine retinal microvascular endothelial cells, identifying the astroglial cell as the likely effector of progesterone-mediated inhibition. Astroglial cells were further implicated as the effectors of steroid-mediated inhibition because none of the steroids inhibited astroglial-independent capillary-like structure formation in response to a reconstituted extracellular matrix, Matrigel. These findings are evidence that steroids modulate neural microvascular endothelial cell functions indirectly through perivascular astrocytes via a receptor-mediated mechanism.

Animals↗

PubMed1977

The close interrelationship between increased vascular retinal permeability and blood pressure level. Evidence from retinal fluorangiography.

A long-term study was done by means of interative fluorangiography on microvascular retinal permeability versus the blood pressure control carried out in 11 patients with a diastolic blood pressure of greater than or equal to 130 mm Hg and with retinal exudates, haemorrhages and oedema. No matter what the original disease was (i.e., essential, renovascular, endocrine hypertension or chronic nephropathy with terminal renal failure) the increased permeability appeared to be critically connected with the blood pressure level. Our results confirm that hypertension per se might be the cause of vascular permeability changes.

Adult↗

PubMed1979

Retinal fluorescein angiography and hemoglobin A1C in borderline diabetes.

In a controlled study fluorescein angiography of the retina and measurements of hemoglobin A1C were carried out in subjects with slightly abnormal two-hour glucose tolerance and controls with normal glucose tolerance. Fluorescent dots were present in 50 per cent of the series with a reduced glucose tolerance. Leakage from retinal vessels was noted in 20 per cent. In the control group fluorescent dots were present in 25 per cent, of whom none showed leakage. In neither of the series did any subject display ophthalmoscopically visible signs of diabetic retinopathy. In the subjects with abnormal glucose tolerance the mean concentration of hemoglobin A1C was 5.88% +/- 1.15 (SD) and in the control group 5.11% +/- 0.85 (SD) (P less than 0.05) . No correlation was demonstrable between the number of fluorescent dots, hemoglobin A1C and age in the group with abnormal glucose tolerance, but a relationship was noticed between a hereditary disposition to diabetes mellitus and presence of fluorescent dots. Smoking appeared not to have any influence. The result of the present study indicates that incipient retinal microvascular changes and evidence of an early breakdown of the blood-retinal barrier may be present in subjects before diabetes becomes manifest.

Diabetes Mellitus↗

PubMed1990

Astrocytes induce neural microvascular endothelial cells to form capillary-like structures in vitro.

Astrocytes maintain a unique association with the central nervous system microvasculature and are thought to play a role in neural microvessel formation and differentiation. We investigated the influence of astroglial cells on neural microvascular endothelial differentiation in vitro. Using an astroglial-endothelial coculture system, rat brain astrocytes and C6 cells of astroglial lineage are shown to induce bovine retinal microvascular endothelial (BRE) cells to form capillary-like structures. Light microscopic evidence for endothelial reorganization began within 48 hours and was complete 72-96 hours following the addition of BRE cells to 1-day-old astroglial cultures. The extent of BRE reorganization was quantitated by computer-assisted analysis and shown to be dependent upon the density of both the BRE and C6 cells within the cocultures. Coculture conditions in which BRE cells were separated from C6 cells by porous membranes failed to generate this endothelial cell change. Likewise, C6-conditioned media and C6-endothelial coculture conditioned media did not induce BRE cell reorganization. Extracellular laminin within the C6-endothelial cocultures, identified by indirect immunofluorescence, was concentrated at the endothelial-astroglial interface of capillary-like structures consistent with incipient basement membrane formation. Astroglial cells accumulated adjacent to capillary-like structures suggesting the presence of bidirectional influences between the reorganized endothelial cells and astroglia. This is the first demonstration of astroglial induction of angiogenesis in vitro and these findings support a functional role for perivascular astrocytes in the vascularization of neural tissue such as retina and brain.

Animals↗

PubMed1992

[Retinal microangiopathies in diabetic children and adolescents, occurring in cases of pubertal and prepubertal onset of diabetes].

The prevalence and development of retinal microvascular complications in pre-puberty and puberty onset insulin-dependent diabetes mellitus were studied in 109 young patients with an average follow-up of 6 years. The data suggest that the earlier childhood the diabetes began, the later the microvascular abnormalities could be found by fluorescein angiography. First signs of background retinopathy were seen in average 20--22 years of age, almost independently the age at onset of diabetes. Rapid progression of retinal vascular damage occurred mainly in postpubertal but not pubertal subjects. Diabetes with puberty onset meant worse prognosis in the respect of retinal vascular complications than pre-puberty onset. Good glycemic control would be achieved more difficult in subjects with puberty onset diabetes added to a changing hormonal balance. The authors suggest that psychological factors (altered behavior during and after puberty) and other problems of adolescents (changes in social, familial and working conditions) may also contribute to poor glycemic control. Though the effect of prepubertal duration on the risk of retinal complications appears to be smaller than later years, the attendant work in prepubertal years is as important as later.

Adolescent↗

PubMed1990

Quantitative determination of skin thickness in diabetes mellitus: relationship to disease parameters.

It has been suggested that thick skin on the dorsum of the hands and fingers is a common finding in diabetes mellitus, and that affected persons have an increased prevalence of diabetic retinal microvascular disease. Using high resolution ultrasonography, we were able to quantitatively demonstrate increased skin thickness on the hands and feet of many of our diabetic patients. In our limited series, however, there was no correlation with retinal disease. The general occurrence of thick skin on the extremities of persons with diabetes mellitus is apparently independent from the thick skin syndromes which are associated with disease complications.

Adult↗