Cilioretinal Arteries and Cilioretinal Veins in Eyes with Pathologic Myopia.
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ABSTRACT:
SUBMITTER: Watanabe T
PROVIDER: S-EPMC6384956 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Purpose: To develop a photographic classification for cilioretinal arteries and to investigate its association with myopic macular degeneration (MMD). Methods: One thousand six hundred ninety-two highly myopic eyes of 1,692 patients were included. The presence of a cilioretinal artery was determined by fundus photographs, and a photographic classification was proposed. MMD was classified according to the International META-PM Classification. Associations of the cilioretinal artery and its classifications with MMD and visual acuity were analyzed. Results: Of the eyes tested, 245 (14.5%) had a cilioretinal artery. The cilioretinal arteries were classified into four categories (temporal "cake-fork," 35.92%; temporal "ribbon," 53.47%; "multiple," 6.53%; "nasal," 4.08%) and 3 distributions based on whether its visible branches reached the central foveal area. Eyes with cilioretinal arteries had significantly less MMD of grade ≥3 and better visual acuity than those without (P < 0.01). Multiple linear regression analysis showed that younger age, male sex, shorter axial length, and the presence of a cilioretinal artery were associated with better visual acuity in highly myopic eyes (all P < 0.05). The "nasal" category presented more MMD with grade ≥3 and worse visual acuity than the other categories (P < 0.05), whereas the "multiple" category contained no eyes with MMD grade ≥3. The cilioretinal arteries reaching the central foveal area showed less MMD of grade ≥3 and better visual acuity than those not (P < 0.05). Conclusions: We propose a photographic classification for cilioretinal arteries that has good clinical relevance to visual functions. The cilioretinal artery may potentially afford protection against MMD.
| S-EPMC7738318 | biostudies-literature
Project description:Arteries and veins have very different susceptibility to certain vascular diseases such as atherosclerosis and vascular calcification. The molecular mechanisms of these differences are not fully understood. In this study, we discovered that COUP-TFII, a transcription factor critical for establishing the venous identity during embryonic vascular development, also regulates the pathophysiological functions of adult blood vessels, especially those directly related to vascular diseases. Specifically, we found that suppression of COUP-TFII in venous ECs switched its phenotype toward pro-atherogenic by up-regulating the expression of inflammatory genes and down-regulating anti-thrombotic genes. ECs with COUP-TFII knockdown also readily undergo endothelial-to-mesenchymal transition (EndoMT) and subsequent osteogenic differentiation with dramatically increased osteogenic transcriptional program and calcium deposition. Consistently, over-expression of COUP-TFII led to the completely opposite effects. In vivo validation of these pro-atherogenic and osteogenic genes also demonstrates a broad consistent differential expression pattern in mouse aorta vs. vena cava ECs, which cannot be explained by the difference in hemodynamic flow. These data reveal phenotypic modulation by different levels of COUP-TFII in arterial and venous ECs, and suggest COUP-TFII may play an important role in the different susceptibilities of arteries and veins to vascular diseases such as atherosclerosis and vascular calcification.
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Project description:We investigated birefringence-derived scleral artifacts in optical coherence tomography (OCT) images of eyes with pathologic myopia. This study included 76 eyes of 42 patients with pathologic myopia. Five sets of OCT B-scan images of the macula were obtained using commercial swept-source OCT. A dataset of prototype swept-source polarization-diversity OCT images was used to identify polarization-dependent OCT images (i.e., complex averaging of OCT signals from two polarization channels) and polarization-independent OCT images (i.e., intensity averaging of two OCT signals). Polarization-dependent OCT images and commercial OCT images were assessed for the presence of birefringence-derived artifacts by comparison with polarization-independent OCT images. Both polarization-dependent OCT images and commercial OCT images contained scleral vessel artifacts. Scleral vessel artifacts were present in 46 of 76 eyes (60.5%) imaged by polarization-dependent OCT and 17 of 76 eyes (22.4%) imaged by commercial OCT. The proportion of images that showed scleral vessel artifacts was significantly greater among polarization-dependent OCT images than among commercial OCT images (P < 0.001). Additionally, polarization-dependent OCT images showed low-intensity band artifacts. This study demonstrated the existence of birefringence-derived scleral artifacts in commercial OCT images and indicated that polarization-diversity OCT is an effective tool to evaluate the presence of these artifacts.
| S-EPMC9669004 | biostudies-literature
Project description:PurposeTo report the detection of retrobulbar blood vessel in the optical coherence tomography angiographic (OCTA) images of two eyes with pathologic myopia.ObservationsTwo eyes of 2 cases with pathologic myopia were examined by OCTA (RTVue XR Avanti, Optovue, and Cirrus 5000, Zeiss). Case 1 was a 64-year-old man, and Case 2 was a 65-year-old woman. In Case 1, the thickness of the subfoveal choroid was 38 μm and the sclera was 274 μm, and they were 17 μm and 214 μm, respectively, in Case 2. The axial length was 35.8 mm in Case 1 and 29.5 mm in Case 2. The choroidal vessels were clearly visible in the choriocapillary slab in both the RTVue and the Cirrus images. The vessels were visible in the area of the retinal pigment epithelial and choriocapillaris atrophy due to the pathologic myopia. The retrobulbar blood vessels temporal to fovea were seen in the OCTA images at the level of the outer aspect of the sclera in both cases. Cross sectional images of the retrobulbar blood vessel in both cases were observed under the sclera in serial scan images overlaid with blood flow.Conclusionsand Importance: These in situ images of the retrobulbar blood vessels that were obtained by OCTA was possible because of the thinness of the choroid and sclera and atrophy of the choriocapillaris in these eyes with pathologic myopia. We conclude that OCTA might have utility to study the retrobulbar vascular alterations in eyes with pathologic myopia.
| S-EPMC5757478 | biostudies-literature
Project description:PurposeTo establish the prevalence and heritability of cilioretinal arteries (CRAs), tilted discs (TDs) and situs inversus (SI).MethodsFundus photos from the Twins UK Adult Twin registry twin database were analyzed: 1812 individuals, 526 complete monozygotic (MZ) twin pairs and 336 complete dizygotic (DZ) pairs. Images were assessed non-stereoscopically on a computer screen by the same ophthalmologist for presence of CRAs, TDs or SI. Prevalence figures, probandwise concordances and heritabilities were calculated.ResultsPrevalence of a CRA in subjects' right eyes was 28.6% (26.5-30.8). Prevalence of subjects with a CRA in at least one eye was 45.0% (42.6-47.5), with a TD in at least one eye was 1.2% (0.8-1.9), and with SI at least one eye was 0.5% (0.3-1.0). There was no association between birth weight and presence of CRA. Concordance for CRA in at least one eye (MZ twins) was 60% (95% CI 55-64), and (DZ) was 45% (95% CI 39-51). Heritability for CRAs in at least one eye was 49.4% (95% CI 38.1-59.7) and for both eyes was 32.9% (95% CI 10.4-53.3). We were unable to calculate meaningful heritabilities or concordances for TDs and situs SI, due to insufficient numbers.ConclusionsThe presence of CRAs appears to be moderately heritable, with greater variance explained by individual environmental factors or even stochastic events. They were not associated with low birth weight. Future genetic research and studies of birth/lifecourse cohorts may offer further insights into the etiology of congenital papillovascular abnormalities.
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Project description:This experiment compares veins with arteries using microarrays.
2008-03-10 | E-TABM-368 | biostudies-arrayexpress
Project description:The principal function of the lymphatic system is to transport lymph from the interstitium to the nodes and then from the nodes to the blood. In doing so lymphatics play important roles in fluid homeostasis, macromolecular/antigen transport and immune cell trafficking. To better understand the genes that contribute to their unique physiology, we compared the transcriptional profile of muscular lymphatics (prenodal mesenteric microlymphatics and large, postnodal thoracic duct) to axillary and mesenteric arteries and veins isolated from rats. Clustering of the differentially expressed genes demonstrated that the lymph versus blood vessel differences were more profound than between blood vessels, particularly the microvessels. Gene ontology functional category analysis indicated that microlymphatics were enriched in antigen processing/presentation, IgE receptor signaling, catabolic processes, translation and ribosome; while they were diminished in oxygen transport, regulation of cell proliferation, glycolysis and inhibition of adenylate cyclase activity by G-proteins. We evaluated the differentially expressed microarray genes/products by qPCR and/or immunofluorescence. Immunofluorescence documented that multiple MHC class II antigen presentation proteins were highly expressed by an antigen-presenting cell (APC) type found resident within the lymphatic wall. These APCs also expressed CD86, a co-stimulatory protein necessary for T-cell activation. We evaluated the distribution and phenotype of APCs within the pre and postnodal lymphatic network. This study documents a novel population of APCs resident within the walls of muscular, prenodal lymphatics that indicates novel roles in antigen sampling and immune responses. In conclusion, these prenodal lymphatics exhibit a unique profile that distinguishes them from blood vessels and highlights the role of the lymphatic system as an immunovascular system linking the parenchymal interstitium, lymph nodes and the blood.
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Project description:Introduction: The study examined the behavior of vasculature in conditions of eliminated cardiac function using mathematical modeling. In addition, we addressed the question of whether the stretch-recoil capability of veins, at least in part accounts for the slower response to simulated cardiac arrest. Methods: In the first set of computational experiments, blood flow and pressure patterns in veins and arteries during the first few seconds after cardiac arrest were assessed via a validated multi-scale mathematical model of the whole cardiovascular system, comprising cardiac dynamics, arterial and venous blood flow dynamics, and microcirculation. In the second set of experiments, the effects of stretch-recoil zones of venous vessels with different diameters and velocities on blood velocity and dynamic pressure analyzed using computational fluid dynamics (CFD) modeling. Results: In the first set of experiments, measurement of changes in velocity, dynamic pressure, and fluid flow revealed that the venous system responded to cardiac arrest more slowly compared to the arteries. This disparity might be due to the intrinsic characteristics of the venous system, including stretch-recoil and elastic fiber composition. In the second set of experiments, we attempted to determine the role of the stretch-recoil capability of veins in the slower response to cardiac arrest. During the second set of experiments, we found that this recoil behavior increased dynamic pressure, velocity, and blood flow. The enhancement in dynamic pressure through combining the results from both experiments yielded a 15-40% increase in maximum dynamic pressure due to stretch-recoil, depending on vein diameter under normal conditions. Conclusion: In the situation of cardiac arrest, the vein geometry changes continue, promoting smooth responses of the venous system. Moreover, the importance of such vein behavior in blood displacement may grow as the pressure on the venous side gradually decreases with time. Our experiments suggest that the driving force for venous return is the pressure difference that remains within the venous system after the energy coming from every ventricular systole spent to overcome the resistance created by arterial and capillary systems.
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Project description:BACKGROUND:The incidence of acute cardiovascular complications is highly time-of-day dependent. However, the mechanisms driving rhythmicity of ischemic vascular events are unknown. Although enhanced numbers of leukocytes have been linked to an increased risk of cardiovascular complications, the role that rhythmic leukocyte adhesion plays in different vascular beds has not been studied. METHODS:We evaluated leukocyte recruitment in vivo by using real-time multichannel fluorescence intravital microscopy of a tumor necrosis factor-?-induced acute inflammation model in both murine arterial and venous macrovasculature and microvasculature. These approaches were complemented with genetic, surgical, and pharmacological ablation of sympathetic nerves or adrenergic receptors to assess their relevance for rhythmic leukocyte adhesion. In addition, we genetically targeted the key circadian clock gene Bmal1 (also known as Arntl) in a lineage-specific manner to dissect the importance of oscillations in leukocytes and components of the vessel wall in this process. RESULTS:In vivo quantitative imaging analyses of acute inflammation revealed a 24-hour rhythm in leukocyte recruitment to arteries and veins of the mouse macrovasculature and microvasculature. Unexpectedly, although in arteries leukocyte adhesion was highest in the morning, it peaked at night in veins. This phase shift was governed by a rhythmic microenvironment and a vessel type-specific oscillatory pattern in the expression of promigratory molecules. Differences in cell adhesion molecules and leukocyte adhesion were ablated when disrupting sympathetic nerves, demonstrating their critical role in this process and the importance of ?2-adrenergic receptor signaling. Loss of the core clock gene Bmal1 in leukocytes, endothelial cells, or arterial mural cells affected the oscillations in a vessel type-specific manner. Rhythmicity in the intravascular reactivity of adherent leukocytes resulted in increased interactions with platelets in the morning in arteries and in veins at night with a higher predisposition to acute thrombosis at different times as a consequence. CONCLUSIONS:Together, our findings point to an important and previously unrecognized role of artery-associated sympathetic innervation in governing rhythmicity in vascular inflammation in both arteries and veins and its potential implications in the occurrence of time-of-day-dependent vessel type-specific thrombotic events.
| S-EPMC6756975 | biostudies-literature
Project description:The vasculature of the central nervous system (CNS) is composed of vascular endothelial and mural cells which interact closely with glial cells and neurons. The development of the CNS vascularisation is a unique process which requires the contribution of specific regulators in addition to the classical angiogenic factors. The egfl7 gene is mainly detected in endothelial cells during physiological and pathological angiogenesis. Egfl7 codes for a secreted protein which predominantly accumulates into the extracellular space where it controls vascular elastin deposition or the Notch pathway. Egfl7 is the host gene of the microRNA miR126 which is also expressed in endothelial cells and which plays major functions during blood vessel development. While the expression of egfl7 and that of miR126 were well described in endothelial cells during development, their pattern of expression during the establishment of the CNS vasculature is still unknown. By analysing the expression of egfl7 and miR126 during mouse retina vascularisation, we observed that while expression of miR126 is detected in all endothelia, egfl7 is initially expressed in all endothelial cells and then is progressively restricted to veins and to their neighbouring capillaries. The recruitment of mural cells around retina arteries coincides with the down-regulation of egfl7 in the arterial endothelial cells, suggesting that this recruitment could be involved in the loss of egfl7 expression in arteries. However, the expression pattern of egfl7 is similar when mural cell recruitment is prevented by the injection of a PDGFR? blocking antibody, suggesting that vessel maturation is not responsible for egfl7 down-regulation in retinal arteries.
| S-EPMC3942447 | biostudies-literature