scholarly journals Effect of VEGF Trap on Normal Retinal Vascular Development and Oxygen-Induced Retinopathy in the Dog

2011 ◽  
Vol 52 (7) ◽  
pp. 4039 ◽  
Author(s):  
Gerard A. Lutty ◽  
D. Scott McLeod ◽  
Imran Bhutto ◽  
Stanley J. Wiegand
Keyword(s):  
Vascular Development ◽  
Oxygen Induced Retinopathy ◽  
Vegf Trap

scholarly journals Simultaneous Fluorescein Angiography and Spectral Domain Optical Coherence Tomography Correlate Retinal Thickness Changes to Vascular Abnormalities in an In Vivo Mouse Model of Retinopathy of Prematurity

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Olachi J. Mezu-Ndubuisi ◽  
Lauren K. Taylor ◽  
Jamee A. Schoephoerster
Keyword(s):  
Optical Coherence Tomography ◽  
Fluorescein Angiography ◽  
Retinopathy Of Prematurity ◽  
Retinal Thickness ◽  
Vascular Development ◽  
Spectral Domain ◽  
Optical Coherence ◽  
Vascular Abnormalities ◽  
Oxygen Induced Retinopathy

Background. Retinopathy of prematurity (ROP) is a condition of abnormal retinal vascular development (RVD) in premature infants. Fluorescein angiography (FA) has depicted phases (early, mid, late, and mature) of RVD in oxygen-induced retinopathy (OIR) mice. We sought to establish the relationship between retinal structural and vascular changes using simultaneous FA and spectral domain optical coherence tomography (SD-OCT). Method. 63 mice were exposed to 77% oxygen at postnatal day 7 (P7) for 5 days, while 63 mice remained in room air (RA). Total retinal thickness (TRT), inner retinal thickness (IRT), and outer retinal thickness (ORT) were calculated at early (P19), mid (P24), late (P32), and mature (P47) phases of RVD. Results. TRT was reduced in OIR (162.66 ± 17.75 μm, n=13) compared to RA mice at P19 (197.57 ± 3.49 μm, n=14), P24, P32, and P49 (P<0.0001). ORT was similar in RA and OIR mice at all ages (P>0.05). IRT was reduced in OIR (71.60 ± 17.14 μm) compared to RA (103.07 ± 3.47 μm) mice at P19 and all ages (P<0.0001). Conclusion. We have shown the spatial and temporal relationship between retinal structure and vascular development in OIR. Significant inner retinal thinning in OIR mice persisted despite revascularization of the capillary network; further studies will elucidate its functional implications in ROP.

scholarly journals Role of Nrf2 in retinal vascular development and the vaso-obliterative phase of oxygen-induced retinopathy

2010 ◽  
Vol 90 (4) ◽  
pp. 493-500 ◽  
Author(s):  
Koichi Uno ◽  
Tarl W. Prow ◽  
Imran A. Bhutto ◽  
Adi Yerrapureddy ◽  
D. Scott McLeod ◽  
...  
Keyword(s):  
Vascular Development ◽  
Oxygen Induced Retinopathy

scholarly journals Amino acid transporter SLC38A5 regulates developmental and pathological retinal angiogenesis

2021 ◽  
Author(s):  
Zhongxiao Wang ◽  
Felix Yemanyi ◽  
Shuo Huang ◽  
Chi-Hsiu Liu ◽  
William R. Britton ◽  
...  
Keyword(s):  
Amino Acid ◽  
Vascular Endothelium ◽  
Vascular Development ◽  
Growth Factor Receptor ◽  
Sprouting Angiogenesis ◽  
Oxygen Induced Retinopathy ◽  
Retinal Blood Vessels ◽  
Retinal Angiogenesis ◽  
Proliferative Retinopathies ◽  
Endothelial Growth Factor

Amino acid metabolism in vascular endothelium is important for sprouting angiogenesis. SLC38A5(solute carrier family 38 member 5), an amino acid (AA) transporter, shuttles neutral AAs across cell membrane, including glutamine, which may serve as metabolic fuel for proliferating endothelial cells (ECs) to promote angiogenesis. Here we found that SLC38A5 is highly enriched in normal retinal vascular endothelium, and more specifically in pathological sprouting neovessels. SLC38A5 is suppressed in retinal blood vessels from Lrp5-/-and Ndpy/- mice, both genetic models of defective retinal vascular development with Wnt signaling mutations. Additionally, Slc38a5 transcription is directly regulated by Wnt/β-catenin signaling. Genetic deficiency of SLC38A5 in mice substantially delays retinal vascular development and suppresses pathological neovascularization in oxygen-induced retinopathy modeling ischemic proliferative retinopathies. Inhibition of SLC38A5 in retinal vascular ECs impairs EC proliferation and angiogenic function, suppresses glutamine uptake, and dampens vascular endothelial growth factor receptor 2 (VEGFR2). Together these findings suggest that SLC38A5 is a new metabolic regulator of retinal angiogenesis by controlling AA nutrient uptake and homeostasis in ECs.

scholarly journals Progenitor cell combination normalizes retinal vascular development in the oxygen-induced retinopathy (OIR) model

JCI Insight ◽  
2019 ◽  
Vol 4 (21) ◽  
Author(s):  
Sergio Li Calzi ◽  
Lynn C. Shaw ◽  
Leni Moldovan ◽  
William C. Shelley ◽  
Xiaoping Qi ◽  
...  
Keyword(s):  
Progenitor Cell ◽  
Vascular Development ◽  
Oxygen Induced Retinopathy

scholarly journals Natriuretic Peptides Attenuate Retinal Pathological Neovascularization Via Cyclic Guanosine Monophosphate Signaling in Pericytes and Astrocytes

2020 ◽  
Vol 40 (1) ◽  
pp. 159-174 ◽  
Author(s):  
Katarina Špiranec Spes ◽  
Sabrina Hupp ◽  
Franziska Werner ◽  
Franziska Koch ◽  
Katharina Völker ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Vascular Development ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Oxygen Induced Retinopathy ◽  
Proliferative Retinopathies

Objective: In proliferative retinopathies, complications derived from neovascularization cause blindness. During early disease, pericyte’s apoptosis contributes to endothelial dysfunction and leakage. Hypoxia then drives VEGF (vascular endothelial growth factor) secretion and pathological neoangiogenesis. Cardiac ANP (atrial natriuretic peptide) contributes to systemic microcirculatory homeostasis. ANP is also formed in the retina, with unclear functions. Here, we characterized whether endogenously formed ANP regulates retinal (neo)angiogenesis. Approach and Results: Retinal vascular development and ischemia-driven neovascularization were studied in mice with global deletion of GC-A (guanylyl cyclase-A), the cGMP (cyclic guanosine monophosphate)-forming ANP receptor. Mice with a floxed GC-A gene were interbred with Tie2-Cre, GFAP-Cre, or PDGF-Rβ-Cre ERT2 lines to dissect the endothelial, astrocyte versus pericyte-mediated actions of ANP in vivo. In neonates with global GC-A deletion (KO), vascular development was mildly delayed. Moreover, such KO mice showed augmented vascular regression and exacerbated ischemia-driven neovascularization in the model of oxygen-induced retinopathy. Notably, absence of GC-A in endothelial cells did not impact retinal vascular development or pathological neovascularization. In vitro ANP/GC-A/cGMP signaling, via activation of cGMP-dependent protein kinase I, inhibited hypoxia-driven astrocyte’s VEGF secretion and TGF-β (transforming growth factor beta)–induced pericyte apoptosis. In neonates lacking ANP/GC-A signaling in astrocytes, vascular development and hyperoxia-driven vascular regression were unaltered; ischemia-induced neovascularization was modestly increased. Remarkably, inactivation of GC-A in pericytes retarded physiological retinal vascularization and markedly enhanced cell apoptosis, vascular regression, and subsequent neovascularization in oxygen-induced retinopathy. Conclusions: Protective pericyte effects of the ANP/GC-A/cGMP pathway counterregulate the initiation and progression of experimental proliferative retinopathy. Our observations indicate augmentation of endogenous pericyte ANP signaling as target for treatment of retinopathies associated with neovascularization.

Effect(s) of Preterm Birth on Normal Retinal Vascular Development and Oxygen-Induced Retinopathy in the Neonatal Rat

2013 ◽  
Vol 38 (12) ◽  
pp. 1266-1273 ◽  
Author(s):  
Rong Li ◽  
Xiangmin Yang ◽  
Yusheng Wang ◽  
Zhaojie Chu ◽  
Tao Liu ◽  
...  
Keyword(s):  
Preterm Birth ◽  
Vascular Development ◽  
Neonatal Rat ◽  
Oxygen Induced Retinopathy

The role of placental growth factor in regulating fetal brain vascular development

2014 ◽  
Author(s):  
Matthew T Ratsep ◽  
Bruno Zavan ◽  
Nicki Peterson ◽  
Leandra Tolusso ◽  
Vanessa Kay ◽  
...  
Keyword(s):  
Growth Factor ◽  
Vascular Development ◽  
Fetal Brain ◽  
Placental Growth Factor
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