Academic literature on the topic 'Retinal vascular remodeling'
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Journal articles on the topic "Retinal vascular remodeling":
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Ricard, Nicolas, Delphine Ciais, Sandrine Levet, Mariela Subileau, Christine Mallet, Teresa A. Zimmers, Se-Jin Lee, Marie Bidart, Jean-Jacques Feige, and Sabine Bailly. "BMP9 and BMP10 are critical for postnatal retinal vascular remodeling." Blood 119, no. 25 (June 21, 2012): 6162–71. http://dx.doi.org/10.1182/blood-2012-01-407593.
Abstract:
Abstract ALK1 is a type I receptor of the TGF-β family that is involved in angiogenesis. Circulating BMP9 was identified as a specific ligand for ALK1 inducing vascular quiescence. In this work, we found that blocking BMP9 with a neutralizing antibody in newborn mice significantly increased retinal vascular density. Surprisingly, Bmp9-KO mice did not show any defect in retinal vascularization. However, injection of the extracellular domain of ALK1 impaired retinal vascularization in Bmp9-KO mice, implicating another ligand for ALK1. Interestingly, we detected a high level of circulating BMP10 in WT and Bmp9-KO pups. Further, we found that injection of a neutralizing anti-BMP10 antibody to Bmp9-KO pups reduced retinal vascular expansion and increased vascular density, whereas injection of this antibody to WT pups did not affect the retinal vasculature. These data suggested that BMP9 and BMP10 are important in postnatal vascular remodeling of the retina and that BMP10 can substitute for BMP9. In vitro stimulation of endothelial cells by BMP9 and BMP10 increased the expression of genes involved in the Notch signaling pathway (Jagged1, Dll4, Hey1, Hey2, Hes1) and decreased apelin expression, suggesting a possible cross-talk between these pathways and the BMP pathway.
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VUGLER, ANTHONY A., MA'AYAN SEMO, ANNA JOSEPH, and GLEN JEFFERY. "Survival and remodeling of melanopsin cells during retinal dystrophy." Visual Neuroscience 25, no. 2 (March 2008): 125–38. http://dx.doi.org/10.1017/s0952523808080309.
Abstract:
AbstractThe melanopsin positive, intrinsically photosensitive retinal ganglion cells (ipRGCs) of the inner retina have been shown to send wide-ranging projections throughout the brain. To investigate the response of this important cell type during retinal dystrophy, we use the Royal College of Surgeons (RCS) dystrophic rat, a major model of retinal degeneration. We find that ipRGCs exhibit a distinctive molecular profile that remains unaltered during early stages of outer retinal pathology (15 weeks of age). In particular, these cells express βIII tubulin, α-acetylated tubulin, and microtubule-associated proteins (MAPs), while remaining negative for other RGC markers such as neurofilaments, calretinin, and parvalbumin. By 14 months of age, melanopsin positive fibers invade ectopic locations in the dystrophic retina and ipRGC axons/dendrites become distorted (a process that may involve vascular remodeling). The morphological abnormalities in melanopsin processes are associated with elevated immunoreactivity for MAP1b and a reduction in α-acetylated tubulin. Quantification of ipRGCs in whole mounts reveals reduced melanopsin cell number with increasing age. Focusing on the retinal periphery, we find a significant decline in melanopsin cell density contrasted by a stability of melanopsin positive processes. In addition to these findings, we describe for the first time, a distinct plexus of melanopsin processes in the far peripheral retina, a structure that is coincident with a short wavelength opsin cone-enriched rim. We conclude that some ipRGCs are lost in RCS dystrophic rats as the disease progresses and that this loss may involve vascular remodeling. However, a significant number of melanopsin positive cells survive into advanced stages of retinal degeneration and show indications of remodeling in response to pathology. Our findings underline the importance of early intervention in human retinal disease in order to preserve integrity of the inner retinal photoreceptive network.
3
Touyz, Rhian M. "Vascular Remodeling, Retinal Arteries, and Hypertension." Hypertension 50, no. 4 (October 2007): 603–4. http://dx.doi.org/10.1161/hypertensionaha.107.095638.
4
García-Ayuso, Diego, Johnny Di Pierdomenico, Manuel Vidal-Sanz, and María P. Villegas-Pérez. "Retinal Ganglion Cell Death as a Late Remodeling Effect of Photoreceptor Degeneration." International Journal of Molecular Sciences 20, no. 18 (September 19, 2019): 4649. http://dx.doi.org/10.3390/ijms20184649.
Abstract:
Inherited or acquired photoreceptor degenerations, one of the leading causes of irreversible blindness in the world, are a group of retinal disorders that initially affect rods and cones, situated in the outer retina. For many years it was assumed that these diseases did not spread to the inner retina. However, it is now known that photoreceptor loss leads to an unavoidable chain of events that cause neurovascular changes in the retina including migration of retinal pigment epithelium cells, formation of “subretinal vascular complexes”, vessel displacement, retinal ganglion cell (RGC) axonal strangulation by retinal vessels, axonal transport alteration and, ultimately, RGC death. These events are common to all photoreceptor degenerations regardless of the initial trigger and thus threaten the outcome of photoreceptor substitution as a therapeutic approach, because with a degenerating inner retina, the photoreceptor signal will not reach the brain. In conclusion, therapies should be applied early in the course of photoreceptor degeneration, before the remodeling process reaches the inner retina.
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Benn, Andreas, Florian Alonso, Jo Mangelschots, Elisabeth Génot, Marleen Lox, and An Zwijsen. "BMP-SMAD1/5 Signaling Regulates Retinal Vascular Development." Biomolecules 10, no. 3 (March 23, 2020): 488. http://dx.doi.org/10.3390/biom10030488.
Abstract:
Vascular development is an orchestrated process of vessel formation from pre-existing vessels via sprouting and intussusceptive angiogenesis as well as vascular remodeling to generate the mature vasculature. Bone morphogenetic protein (BMP) signaling via intracellular SMAD1 and SMAD5 effectors regulates sprouting angiogenesis in the early mouse embryo, but its role in other processes of vascular development and in other vascular beds remains incompletely understood. Here, we investigate the function of SMAD1/5 during early postnatal retinal vascular development using inducible, endothelium-specific deletion of Smad1 and Smad5. We observe the formation of arterial-venous malformations in areas with high blood flow, and fewer and less functional tip cells at the angiogenic front. The vascular plexus region is remarkably hyperdense and this is associated with reduced vessel regression and aberrant vascular loop formation. Taken together, our results highlight important functions of SMAD1/5 during vessel formation and remodeling in the early postnatal retina.
6
Yu, Dao-Yi, Valerie A. Alder, Stephen J. Cringle, Er-Ning Su, and Margaret Burns. "Intraretinal oxygen distribution in urethan-induced retinopathy in rats." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 6 (June 1, 1998): H2009—H2017. http://dx.doi.org/10.1152/ajpheart.1998.274.6.h2009.
Abstract:
This study was performed to explore the interaction between chronic neural degeneration and the subsequent vascular remodeling. Weekly urethan administration in rats from birth produces a retinopathy model characterized by photoreceptor degeneration, retinal vascular regression, and retinal pigment epithelium (RPE) neovascularization. We investigated the hypothesis that altered oxygen distribution across the retina and choroid could be involved in the vascular changes seen in this retinopathy. We compared measurements of vitreal, intraretinal, and choroidal oxygen tension ([Formula: see text]) distribution in anesthetized and ventilated control and urethan-treated rats at 8 and 16 wk of age with the use of oxygen-sensitive microelectrodes. Striking differences were observed in both choroidal and intraretinal [Formula: see text]distribution in urethan-treated rats compared with controls. At both ages, intrachoroidal [Formula: see text] was much lower in the urethan-treated rats. In addition, the intraretinal[Formula: see text] distribution across the inner retinal layers was more uniform than normal. A small elevation in[Formula: see text] was present at 8 wk in the inner nuclear layer where subsequent vascular regression occurred, and a small reduction in [Formula: see text] was present at the RPE, which recovered to normal values by 16 wk in regions where RPE vessel networks were first evident. Although the retinal arteries were considerably thinner at both ages in the urethan-treated rats, the vitreal [Formula: see text] profiles and superficial retinal [Formula: see text] remained normal. The unexpected and large reduction in the oxygen delivery from the choroid found in the urethan-treated rats may account for the lack of major hyperoxia within the pathological retina and the lower oxygen tension in the RPE before the vascular proliferation in this region. We propose that tissue [Formula: see text] is an important determinant of the vascular remodeling, which is seen in this model of neural degeneration and that the [Formula: see text]distribution changes described in this study help provide a new view of the pathogenesis of this model.
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Yan, Qi, E. Helene Sage, and Anita E. Hendrickson. "SPARC Is Expressed by Ganglion Cells and Astrocytes in Bovine Retina." Journal of Histochemistry & Cytochemistry 46, no. 1 (January 1998): 3–10. http://dx.doi.org/10.1177/002215549804600102.
Abstract:
SPARC (secreted protein, acidic and rich in cysteine)/osteonectin is a matricellular, counteradhesive glycoprotein that disrupts cell-matrix interactions, interacts with growth factors and components of extracellular matrix, and modulates the cell cycle, but appears to subserve only minor structural roles. SPARC is expressed in a variety of tissues during embryogenesis and remodeling and is believed to regulate vascular morphogenesis and cellular differentiation. Although usually limited in normal adult tissues, SPARC is expressed at significant levels in the adult central nervous system. Using a monoclonal antibody against bovine bone osteonectin, we have determined the localization of SPARC in newborn (3-day-old) and adult (4–8-year-old) normal bovine retinas. SPARC was present in the soma of ganglion cells and strong reactivity was found in ganglion cell axons. Muller cells displayed no immunoreactivity, but SPARC was present in retinal astrocytes that were identified by the astrocyte marker glial fibrillary acidic protein (GFAP). Newborn calf retina showed a staining pattern similar to that of adult retina but exhibited significantly reduced levels of SPARC. Minimal levels of SPARC protein were also detected in some capillaries of the inner retina of both newborn and adult animals, whereas large vessels were negative. The presence of SPARC in the retina was confirmed by Western blotting of retinal extracts. These data indicate that SPARC originating from both neurons and glia of the inner retina may be an important modulator of retinal angiogenesis. The increased expression of SPARC in adult relative to newborn retinal tissue also indicates that SPARC has an ongoing role in the maintainance of retinal functions.
8
Huang, Hu. "Pericyte-Endothelial Interactions in the Retinal Microvasculature." International Journal of Molecular Sciences 21, no. 19 (October 8, 2020): 7413. http://dx.doi.org/10.3390/ijms21197413.
Abstract:
Retinal microvasculature is crucial for the visual function of the neural retina. Pericytes and endothelial cells (ECs) are the two main cellular constituents in the retinal microvessels. Formation, maturation, and stabilization of the micro-vasculatures require pericyte-endothelial interactions, which are perturbed in many retinal vascular disorders, such as retinopathy of prematurity, retinal vein occlusion, and diabetic retinopathy. Understanding the cellular and molecular mechanisms of pericyte-endothelial interaction and perturbation can facilitate the design of therapeutic intervention for the prevention and treatment of retinal vascular disorders. Pericyte-endothelial interactions are indispensable for the integrity and functionality of retinal neurovascular unit (NVU), including vascular cells, retinal neurons, and glial cells. The essential autocrine and paracrine signaling pathways, such as Vascular endothelial growth factor (VEGF), Platelet-derived growth factor subunit B (PDGFB), Notch, Angipointein, Norrin, and Transforming growth factor-beta (TGF-β), have been well characterized for the regulation of pericyte-endothelial interactions in the neo-vessel formation processes (vasculogenesis and angiogenesis) during embryonic development. They also play a vital role in stabilizing and remodeling mature vasculature under pathological conditions. Awry signals, aberrant metabolisms, and pathological conditions, such as oxidative stress and inflammation, can disrupt the communication between pericytes and endothelial cells, thereby resulting in the breakdown of the blood-retinal barrier (BRB) and other microangiopathies. The emerging evidence supports extracellular exosomes’ roles in the (mis)communications between the two cell types. This review summarizes the essential knowledge and updates about new advancements in pericyte-EC interaction and communication, emphasizing the retinal microvasculature.
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Habibi-Kavashkohie, Mohammad Reza, Tatiana Scorza, and Malika Oubaha. "Senescent Cells: Dual Implications on the Retinal Vascular System." Cells 12, no. 19 (September 23, 2023): 2341. http://dx.doi.org/10.3390/cells12192341.
Abstract:
Cellular senescence, a state of permanent cell cycle arrest in response to endogenous and exogenous stimuli, triggers a series of gradual alterations in structure, metabolism, and function, as well as inflammatory gene expression that nurtures a low-grade proinflammatory milieu in human tissue. A growing body of evidence indicates an accumulation of senescent neurons and blood vessels in response to stress and aging in the retina. Prolonged accumulation of senescent cells and long-term activation of stress signaling responses may lead to multiple chronic diseases, tissue dysfunction, and age-related pathologies by exposing neighboring cells to the heightened pathological senescence-associated secretory phenotype (SASP). However, the ultimate impacts of cellular senescence on the retinal vasculopathies and retinal vascular development remain ill-defined. In this review, we first summarize the molecular players and fundamental mechanisms driving cellular senescence, as well as the beneficial implications of senescent cells in driving vital physiological processes such as embryogenesis, wound healing, and tissue regeneration. Then, the dual implications of senescent cells on the growth, hemostasis, and remodeling of retinal blood vessels are described to document how senescent cells contribute to both retinal vascular development and the severity of proliferative retinopathies. Finally, we discuss the two main senotherapeutic strategies—senolytics and senomorphics—that are being considered to safely interfere with the detrimental effects of cellular senescence.
10
Задорожний, Олег, Андрій Король, Ілля Насінник, Тарас Кустрін, Володимир Науменко, and Наталія Пасєчнікова. "Precise in vivo adaptive optics imaging of retinal vessels." Oftalmologicheskii Zhurnal, no. 2 (April 25, 2023): 31–38. http://dx.doi.org/10.31288/oftalmolzh202323138.
Abstract:
Adaptive optics (AO) provides new, unique opportunities for in vivo visualization of retinal vasculature. AO retinal vessel imaging can be utilized as a component of multimodal imaging tools to complement conventional diagnostic imaging modalities. Non-invasive and highly promising AO imaging of fundus structures allows the qualitative and quantitative assessment of early signs of retinal vascular remodeling associated with age, arterial hypertension, diabetes mellitus and other disorders.
Dissertations / Theses on the topic "Retinal vascular remodeling":
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Yang, Tianxiang. "Influence of chronic intermittent hypoxia (CIH) in retinal neovascularization and vascular remodeling." Electronic Thesis or Diss., Sorbonne université, 2024. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2024SORUS059.pdf.
Abstract:
Les rétinopathies néovasculaires et les œdèmes sont des complications menaçant la vue des rétinopathies ischémiques, telles que la rétinopathie du prématuré (ROP) et la rétinopathie diabétique (DR). L'apnée du sommeil qui conduit à une hypoxie chronique intermittente (CIH) est un facteur de risque indépendant de maladie grave, mais les mécanismes sous-jacents sont inconnus. Nous montrons ici que le CIH expérimental pendant la phase ischémique de la rétinopathie induite par l'oxygène chez la souris réduit considérablement la revascularisation bénéfique de la rétine ischémique et augmente la perte neuronale et la néovascularisation pathologique. Mécaniquement, nous démontrons que le CIH réduit à la fois l'expression du facteur de stimulation des colonies 1 (CSF-1) et l'augmentation induite par l'ischémie des cellules microgliales rétiniennes qui favorisent la revascularisation de la rétine ischémique en l'absence de CIH. L'inhibition locale du CSF1R au cours de la rétinopathie ischémique a réduit le nombre de cellules microgliales, inhibé la revascularisation et exacerbé la néovascularisation pathologique, récapitulant plusieurs effets du CIH. Nos résultats fournissent un nouveau mécanisme par lequel l'apnée du sommeil et le CIH aggravent les rétinopathies ischémiques, soulignant l'importance du traitement de l'apnée dans la ROP et la RD pour aider à prévenir une maladie grave menaçant la vueNeovascular retinopathies and edema are sight threatening complications of ischemic retinopathies, such as retinopathy of prematurity (ROP) and diabetic retinopathy (DR). Sleep apnea that leads to chronic intermittent hypoxia (CIH) is an independent risk factor for severe disease, but the underlying mechanisms are unknown. Here we show that experimental CIH during the ischemic phase of oxygen induced retinopathy in mice severely reduces beneficial revascularization of the ischemic retina, and increases neuronal loss and pathological neovascularization. Mechanistically we demonstrate that CIH reduces both colony stimulating factor 1 (CSF-1) expression and the ischemia-induced increase of retinal microglial cells that promotes the revascularization of the ischemic retina in the absence of CIH. Local CSF1R inhibition during ischemic retinopathy reduced the number of microglial cells, inhibited revascularization, and exacerbated pathological neovascularization, recapitulating several effects of CIH. Our findings provide a novel mechanism by which sleep apnea and CIH aggravate ischemic retinopathies, underscoring the importance of treating apnea in ROP and DR to help prevent sight threatening severe disease
2
Ricard, Nicolas. "ALK1 et BMP9 dans le remodelage vasculaire de la génétique humaine aux modèles murins." Phd thesis, Université de Grenoble, 2011. http://tel.archives-ouvertes.fr/tel-00854192.
Abstract:
ALK1 est un récepteur de la famille du TGF-β, principalement exprimé dans les cellules endothéliales. Le ligand physiologique et circulant d'ALK1, BMP9, a été découvert par notre laboratoire en 2007, ce qui a ouvert des possibilités d'étude de la fonction d'ALK1. La première partie de ma thèse a été consacrée à l'analyse fonctionnelle de mutants d'ALK1, retrouvés sur des patients atteints de la maladie de Rendu-Osler de type 2, en réponse à BMP9. Cette étude a permis de : 1) proposer l'haploinsuffisance fonctionnelle comme modèle de la maladie ; 2) développer un test diagnostique pour discriminer les mutations pathogènes des polymorphismes rares, basé sur leur réponse à BMP9 ; 3) d'avoir une meilleure connaissance des acides aminés d'ALK1 importants dans la réponse à BMP9. Un second travail a consisté en la production de la forme mature de BMP9 et du domaine extracellulaire d'ALK1 en vue de l'étude de la structure cristallographique du complexe. L'expression des protéines et leur purification sont en phase d'optimisation. Enfin, un troisième projet consistait en l'analyse du rôle de BMP9 dans l'angiogenèse in vivo. La neutralisation de BMP9 par deux stratégies distinctes induit une augmentation de la densité vasculaire dans la rétine de la souris. Le mécanisme est en cours d'investigation.
Conference papers on the topic "Retinal vascular remodeling":
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Spitz, Kathleen, Ivan Bozic, Vineet Desai, Gopikrishna M. Rao, Lana M. Pollock, Bela Anand-Apte, and Yuankai K. Tao. "Longitudinal visualization of vascular occlusion, reperfusion, and remodeling in a zebrafish model of retinal vascular leakage using OCT angiography." In SPIE BiOS, edited by Fabrice Manns, Per G. Söderberg, and Arthur Ho. SPIE, 2017. http://dx.doi.org/10.1117/12.2252418.
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Tao, Yuankai K., Xiaoyue Li, Kathleen Spitz, and Ivan Bozic. "Multimodality optical coherence tomography and fluorescence confocal scanning laser ophthalmoscopy in a zebrafish model of retinal vascular occlusion and remodeling." In Ophthalmic Technologies XXVIII, edited by Fabrice Manns, Per G. Söderberg, and Arthur Ho. SPIE, 2018. http://dx.doi.org/10.1117/12.2290930.