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Article ; Online: Nogo-A inhibits vascular regeneration in ischemic retinopathy.

Joly, Sandrine / Dejda, Agnieszka / Rodriguez, Léa / Sapieha, Przemyslaw / Pernet, Vincent

2018 Volume 66, Issue 10, Page(s) 2079–2093

Abstract: Nogo-A is a potent glial-derived inhibitor of axon growth in the injured CNS and acts as a negative regulator of developmental angiogenesis by inhibiting vascular endothelial cell migration. However, its function in pathological angiogenesis has never ... ...

Abstract	Nogo-A is a potent glial-derived inhibitor of axon growth in the injured CNS and acts as a negative regulator of developmental angiogenesis by inhibiting vascular endothelial cell migration. However, its function in pathological angiogenesis has never been studied after ischemic injury in the CNS. Using the mouse model of oxygen-induced retinopathy (OIR) which yields defined zones of retinal ischemia, our goal was to investigate the role of Nogo-A in vascular regeneration. We demonstrate a marked upregulation of the Nogo-A receptor sphingosine 1-phosphate receptor 2 in blood vessels following OIR, while Nogo-A is abundantly expressed in surrounding glial cells. Acute inhibition of Nogo-A with function-blocking antibody 11C7 significantly improved vascular regeneration and consequently prevented pathological pre-retinal angiogenesis. Ultimately, inhibition of Nogo-A led to restoration of retinal function as determined by electrophysiological response of retinal cells to light stimulation. Our data suggest that anti-Nogo-A antibody may protect neuronal cells from ischemic damage by accelerating blood vessel repair in the CNS. Targeting Nogo-A by immunotherapy may improve CNS perfusion after vascular injuries.
MeSH term(s)	Angiogenesis Inducing Agents/pharmacology ; Animals ; Disease Models, Animal ; Ischemia/drug therapy ; Ischemia/metabolism ; Ischemia/pathology ; Mice, Inbred C57BL ; Neovascularization, Physiologic/drug effects ; Neovascularization, Physiologic/physiology ; Neuroglia/drug effects ; Neuroglia/metabolism ; Neuroglia/pathology ; Nogo Proteins/antagonists & inhibitors ; Nogo Proteins/immunology ; Nogo Proteins/metabolism ; Receptors, Lysosphingolipid/metabolism ; Regeneration/drug effects ; Regeneration/physiology ; Retinal Diseases/drug therapy ; Retinal Diseases/metabolism ; Retinal Diseases/pathology ; Retinal Vessels/drug effects ; Retinal Vessels/metabolism ; Retinal Vessels/pathology ; Vision, Ocular/drug effects ; Vision, Ocular/physiology
Chemical Substances	Angiogenesis Inducing Agents ; Nogo Proteins ; Receptors, Lysosphingolipid ; Rtn4 protein, mouse ; sphingosine-1-phosphate receptor-2, mouse
Language	English
Publishing date	2018-07-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.23462
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Zs.A 2345: Show issues

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Article ; Online: HIF1α-dependent hypoxia response in myeloid cells requires IRE1α.

Mawambo, Gaëlle / Oubaha, Malika / Ichiyama, Yusuke / Blot, Guillaume / Crespo-Garcia, Sergio / Dejda, Agnieszka / Binet, François / Diaz-Marin, Roberto / Sawchyn, Christina / Sergeev, Mikhail / Juneau, Rachel / Kaufman, Randal J / Affar, El Bachir / Mallette, Frédérick A / Wilson, Ariel M / Sapieha, Przemyslaw

Journal of neuroinflammation

2023 Volume 20, Issue 1, Page(s) 145

Abstract: Cellular adaptation to low oxygen tension triggers primitive pathways that ensure proper cell function. Conditions of hypoxia and low glucose are characteristic of injured tissues and hence successive waves of inflammatory cells must be suited to ... ...

Abstract	Cellular adaptation to low oxygen tension triggers primitive pathways that ensure proper cell function. Conditions of hypoxia and low glucose are characteristic of injured tissues and hence successive waves of inflammatory cells must be suited to function under low oxygen tension and metabolic stress. While Hypoxia-Inducible Factor (HIF)-1α has been shown to be essential for the inflammatory response of myeloid cells by regulating the metabolic switch to glycolysis, less is known about how HIF1α is triggered in inflammation. Here, we demonstrate that cells of the innate immune system require activity of the inositol-requiring enzyme 1α (IRE1α/XBP1) axis in order to initiate HIF1α-dependent production of cytokines such as IL1β, IL6 and VEGF-A. Knockout of either HIF1α or IRE1α in myeloid cells ameliorates vascular phenotypes in a model of retinal pathological angiogenesis driven by sterile inflammation. Thus, pathways associated with ER stress, in partnership with HIF1α, may co-regulate immune adaptation to low oxygen.
MeSH term(s)	Humans ; Protein Serine-Threonine Kinases/genetics ; Endoribonucleases ; Hypoxia ; Oxygen/metabolism ; Myeloid Cells/metabolism ; Inflammation/metabolism ; Hypoxia-Inducible Factor 1, alpha Subunit
Chemical Substances	Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Endoribonucleases (EC 3.1.-) ; Oxygen (S88TT14065) ; Hypoxia-Inducible Factor 1, alpha Subunit
Language	English
Publishing date	2023-06-21
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-023-02793-y
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Article ; Online: The protein tyrosine phosphatase PTPRJ/DEP-1 contributes to the regulation of the Notch-signaling pathway and sprouting angiogenesis.

Fournier, Patrick / Viallard, Claire / Dejda, Agnieszka / Sapieha, Przemyslaw / Larrivée, Bruno / Royal, Isabelle

Angiogenesis

2019 Volume 23, Issue 2, Page(s) 145–157

Abstract: The Dll4-Notch-signaling pathway regulates capillary sprouting via the specification of endothelial tip cells. While VEGF is a potent inducer of Dll4 expression, the intracellular mediators that stimulate its expression remain poorly defined. The protein ...

Abstract	The Dll4-Notch-signaling pathway regulates capillary sprouting via the specification of endothelial tip cells. While VEGF is a potent inducer of Dll4 expression, the intracellular mediators that stimulate its expression remain poorly defined. The protein tyrosine phosphatase PTPRJ/DEP-1 is required for angiogenesis in normal or pathological contexts through its modulation of VEGF signaling. Here, we show that in DEP-1 KO mice, retinas at post-natal day 5 show enlarged blood vessels, as well as an increased number of tip cells and vessel branching points at the migrating front of the vascular plexus. Consistent with these observations, the proliferation of endothelial cells is increased in the retinas of DEP-1 KO mice, as revealed by phospho-histone H3 staining, and increased phosphorylation of ERK1/2 in HUVECs transfected with DEP-1 siRNA. The expression of Dll4 was decreased in retinas of DEP-1 KO mice and was associated with decreased Notch activation. Mechanistically, reduced Dll4 expression in the absence of DEP-1 was correlated with the inhibition of the Src/Akt/β-Catenin-signaling pathway in HUVECs. Conversely, overexpression of WT DEP-1 in cultured endothelial cells, but not of mutants unable to activate Src-dependent signaling, promoted Dll4 expression. Inhibition of Src, Akt, and β-catenin transcriptional activity, leading to the inhibition of Dll4 expression, further suggested that their activation through a DEP-1-dependent pathway was required to promote Dll4 expression in VEGF-stimulated endothelial cells. Altogether, these data demonstrate that DEP-1, via Akt and β-catenin, is a significant promoter of the VEGF-induced Dll4-Notch pathway, and can contribute to the regulation of the tip and stalk cell phenotypes of endothelial cells.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Calcium-Binding Proteins/genetics ; Calcium-Binding Proteins/metabolism ; Endothelial Cells/metabolism ; Mice ; Neovascularization, Physiologic/genetics ; Protein Tyrosine Phosphatases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Receptor-Like Protein Tyrosine Phosphatases, Class 3/metabolism ; Receptors, Notch/metabolism ; Signal Transduction/physiology ; Vascular Endothelial Growth Factor A/metabolism ; beta Catenin/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Calcium-Binding Proteins ; Receptors, Notch ; Vascular Endothelial Growth Factor A ; beta Catenin ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Protein Tyrosine Phosphatases (EC 3.1.3.48) ; Ptprj protein, mouse (EC 3.1.3.48) ; Receptor-Like Protein Tyrosine Phosphatases, Class 3 (EC 3.1.3.48)
Language	English
Publishing date	2019-10-09
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1484717-6
ISSN	1573-7209 ; 0969-6970
ISSN (online)	1573-7209
ISSN	0969-6970
DOI	10.1007/s10456-019-09683-z
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Zs.A 5094: Show issues

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Article ; Online: Therapeutic targeting of cellular senescence in diabetic macular edema: preclinical and phase 1 trial results.

Crespo-Garcia, Sergio / Fournier, Frédérik / Diaz-Marin, Roberto / Klier, Sharon / Ragusa, Derek / Masaki, Lauren / Cagnone, Gael / Blot, Guillaume / Hafiane, Ikhlas / Dejda, Agnieszka / Rizk, Rana / Juneau, Rachel / Buscarlet, Manuel / Chorfi, Sarah / Patel, Priyanka / Beltran, Pedro J / Joyal, Jean-Sebastien / Rezende, Flavio A / Hata, Masayuki /

Nguyen, Alex / Sullivan, Lynne / Damiano, Jason / Wilson, Ariel M / Mallette, Frédérick A / David, Nathaniel E / Ghosh, Anirvan / Tsuruda, Pamela R / Dananberg, Jamie / Sapieha, Przemyslaw

Nature medicine

2024 Volume 30, Issue 2, Page(s) 443–454

Abstract: Compromised vascular endothelial barrier function is a salient feature of diabetic complications such as sight-threatening diabetic macular edema (DME). Current standards of care for DME manage aspects of the disease, but require frequent intravitreal ... ...

Abstract	Compromised vascular endothelial barrier function is a salient feature of diabetic complications such as sight-threatening diabetic macular edema (DME). Current standards of care for DME manage aspects of the disease, but require frequent intravitreal administration and are poorly effective in large subsets of patients. Here we provide evidence that an elevated burden of senescent cells in the retina triggers cardinal features of DME pathology and conduct an initial test of senolytic therapy in patients with DME. In cell culture models, sustained hyperglycemia provoked cellular senescence in subsets of vascular endothelial cells displaying perturbed transendothelial junctions associated with poor barrier function and leading to micro-inflammation. Pharmacological elimination of senescent cells in a mouse model of DME reduces diabetes-induced retinal vascular leakage and preserves retinal function. We then conducted a phase 1 single ascending dose safety study of UBX1325 (foselutoclax), a senolytic small-molecule inhibitor of BCL-xL, in patients with advanced DME for whom anti-vascular endothelial growth factor therapy was no longer considered beneficial. The primary objective of assessment of safety and tolerability of UBX1325 was achieved. Collectively, our data suggest that therapeutic targeting of senescent cells in the diabetic retina with a BCL-xL inhibitor may provide a long-lasting, disease-modifying intervention for DME. This hypothesis will need to be verified in larger clinical trials. ClinicalTrials.gov identifier: NCT04537884 .
MeSH term(s)	Animals ; Mice ; Humans ; Macular Edema/drug therapy ; Macular Edema/etiology ; Diabetic Retinopathy/drug therapy ; Angiogenesis Inhibitors/therapeutic use ; Endothelial Cells ; Senotherapeutics ; Cellular Senescence ; Diabetes Mellitus
Chemical Substances	Angiogenesis Inhibitors ; Senotherapeutics
Language	English
Publishing date	2024-02-06
Publishing country	United States
Document type	Clinical Trial, Phase I ; Journal Article
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/s41591-024-02802-4
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Zs.A 4212: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 39: Show issues

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Article ; Online: Past history of obesity triggers persistent epigenetic changes in innate immunity and exacerbates neuroinflammation.

Science (New York, N.Y.)

2023 Volume 379, Issue 6627, Page(s) 45–62

Abstract: Age-related macular degeneration is a prevalent neuroinflammatory condition and a major cause of blindness driven by genetic and environmental factors such as obesity. In diseases of aging, modifiable factors can be compounded over the life span. We ... ...

Abstract	Age-related macular degeneration is a prevalent neuroinflammatory condition and a major cause of blindness driven by genetic and environmental factors such as obesity. In diseases of aging, modifiable factors can be compounded over the life span. We report that diet-induced obesity earlier in life triggers persistent reprogramming of the innate immune system, lasting long after normalization of metabolic abnormalities. Stearic acid, acting through Toll-like receptor 4 (TLR4), is sufficient to remodel chromatin landscapes and selectively enhance accessibility at binding sites for activator protein-1 (AP-1). Myeloid cells show less oxidative phosphorylation and shift to glycolysis, ultimately leading to proinflammatory cytokine transcription, aggravation of pathological retinal angiogenesis, and neuronal degeneration associated with loss of visual function. Thus, a past history of obesity reprograms mononuclear phagocytes and predisposes to neuroinflammation.
MeSH term(s)	Animals ; Mice ; Cytokines/genetics ; Immunity, Innate/genetics ; Neuroinflammatory Diseases/genetics ; Neuroinflammatory Diseases/immunology ; Obesity/genetics ; Phagocytes/immunology ; Transcription, Genetic ; Macular Degeneration/genetics ; Macular Degeneration/immunology ; Cellular Reprogramming/genetics ; Epigenetic Memory ; Toll-Like Receptor 4/genetics
Chemical Substances	Cytokines ; Tlr4 protein, mouse ; Toll-Like Receptor 4
Language	English
Publishing date	2023-01-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.abj8894
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Zs.A 27: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 77: Show issues

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Article ; Online: Myeloid-resident neuropilin-1 influences brown adipose tissue in obesity.

Diaz-Marin, Roberto / Crespo-Garcia, Sergio / Wilson, Ariel M / Buscarlet, Manuel / Dejda, Agnieszka / Fournier, Frédérik / Juneau, Rachel / Alquier, Thierry / Sapieha, Przemyslaw

Scientific reports

2021 Volume 11, Issue 1, Page(s) 15767

Abstract: The beneficial effects of brown adipose tissue (BAT) on obesity and associated metabolic diseases are mediated through its capacity to dissipate energy as heat. While immune cells, such as tissue-resident macrophages, are known to influence adipose ... ...

Abstract	The beneficial effects of brown adipose tissue (BAT) on obesity and associated metabolic diseases are mediated through its capacity to dissipate energy as heat. While immune cells, such as tissue-resident macrophages, are known to influence adipose tissue homeostasis, relatively little is known about their contribution to BAT function. Here we report that neuropilin-1 (NRP1), a multiligand single-pass transmembrane receptor, is highly expressed in BAT-resident macrophages. During diet-induced obesity (DIO), myeloid-resident NRP1 influences interscapular BAT mass, and consequently vascular morphology, innervation density and ultimately core body temperature during cold exposure. Thus, NRP1-expressing myeloid cells contribute to the BAT homeostasis and potentially its thermogenic function in DIO.
MeSH term(s)	Adipose Tissue, Brown/physiology ; Animals ; Diet/adverse effects ; Energy Metabolism ; Homeostasis ; Macrophages/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myeloid Cells/metabolism ; Neuropilin-1/physiology ; Obesity/etiology ; Obesity/metabolism ; Obesity/pathology ; Obesity/prevention & control ; Thermogenesis
Chemical Substances	Neuropilin-1 (144713-63-3)
Language	English
Publishing date	2021-08-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-95064-w
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Article ; Online: Myeloid-resident neuropilin-1 influences brown adipose tissue in obesity

Roberto Diaz-Marin / Sergio Crespo-Garcia / Ariel M. Wilson / Manuel Buscarlet / Agnieszka Dejda / Frédérik Fournier / Rachel Juneau / Thierry Alquier / Przemyslaw Sapieha

Scientific Reports, Vol 11, Iss 1, Pp 1-

2021 Volume 11

Abstract: Abstract The beneficial effects of brown adipose tissue (BAT) on obesity and associated metabolic diseases are mediated through its capacity to dissipate energy as heat. While immune cells, such as tissue-resident macrophages, are known to influence ... ...

Abstract	Abstract The beneficial effects of brown adipose tissue (BAT) on obesity and associated metabolic diseases are mediated through its capacity to dissipate energy as heat. While immune cells, such as tissue-resident macrophages, are known to influence adipose tissue homeostasis, relatively little is known about their contribution to BAT function. Here we report that neuropilin-1 (NRP1), a multiligand single-pass transmembrane receptor, is highly expressed in BAT-resident macrophages. During diet-induced obesity (DIO), myeloid-resident NRP1 influences interscapular BAT mass, and consequently vascular morphology, innervation density and ultimately core body temperature during cold exposure. Thus, NRP1-expressing myeloid cells contribute to the BAT homeostasis and potentially its thermogenic function in DIO.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2021-08-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Myeloid-resident neuropilin-1 promotes choroidal neovascularization while mitigating inflammation.

Andriessen, Elisabeth M M A / Binet, François / Fournier, Frédérik / Hata, Masayuki / Dejda, Agnieszka / Mawambo, Gaëlle / Crespo-Garcia, Sergio / Pilon, Frédérique / Buscarlet, Manuel / Beauchemin, Karine / Bougie, Véronique / Cumberlidge, Garth / Wilson, Ariel M / Bourgault, Steve / Rezende, Flavio A / Beaulieu, Normand / Delisle, Jean-Sébastien / Sapieha, Przemyslaw

EMBO molecular medicine

2021 Volume 13, Issue 5, Page(s) e11754

Abstract: Age-related macular degeneration (AMD) in its various forms is a leading cause of blindness in industrialized countries. Here, we provide evidence that ligands for neuropilin-1 (NRP1), such as Semaphorin 3A and VEGF-A, are elevated in the vitreous of ... ...

Abstract	Age-related macular degeneration (AMD) in its various forms is a leading cause of blindness in industrialized countries. Here, we provide evidence that ligands for neuropilin-1 (NRP1), such as Semaphorin 3A and VEGF-A, are elevated in the vitreous of patients with AMD at times of active choroidal neovascularization (CNV). We further demonstrate that NRP1-expressing myeloid cells promote and maintain CNV. Expression of NRP1 on cells of myeloid lineage is critical for mitigating production of inflammatory factors such as IL6 and IL1β. Therapeutically trapping ligands of NRP1 with an NRP1-derived trap reduces CNV. Collectively, our findings identify a role for NRP1-expressing myeloid cells in promoting pathological angiogenesis during CNV and introduce a therapeutic approach to counter neovascular AMD.
MeSH term(s)	Angiogenesis Inhibitors ; Choroidal Neovascularization ; Humans ; Inflammation ; Neuropilin-1/genetics ; Vascular Endothelial Growth Factor A ; Visual Acuity ; Wet Macular Degeneration
Chemical Substances	Angiogenesis Inhibitors ; Vascular Endothelial Growth Factor A ; Neuropilin-1 (144713-63-3)
Language	English
Publishing date	2021-04-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2467145-9
ISSN	1757-4684 ; 1757-4676
ISSN (online)	1757-4684
ISSN	1757-4676
DOI	10.15252/emmm.201911754
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Zs.A 6784: Show issues

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Article ; Online: miR-106b suppresses pathological retinal angiogenesis.

Ménard, Catherine / Wilson, Ariel M / Dejda, Agnieszka / Miloudi, Khalil / Binet, François / Crespo-Garcia, Sergio / Parinot, Célia / Pilon, Frédérique / Juneau, Rachel / Andriessen, Elisabeth Mma / Mawambo, Gaëlle / SanGiovanni, John Paul / De Guire, Vincent / Sapieha, Przemyslaw

Aging

2020 Volume 12, Issue 24, Page(s) 24836–24852

Abstract: MicroRNAs are small non-coding RNAs that post-transcriptionally regulate gene expression. We recently demonstrated that levels of miR-106b were significantly decreased in the vitreous and plasma of patients with neovascular age-related macular ... ...

Abstract	MicroRNAs are small non-coding RNAs that post-transcriptionally regulate gene expression. We recently demonstrated that levels of miR-106b were significantly decreased in the vitreous and plasma of patients with neovascular age-related macular degeneration (AMD). Here we show that expression of the miR-106b-25 cluster is negatively regulated by the unfolded protein response pathway of protein kinase RNA-like ER kinase (PERK) in a mouse model of neovascular AMD. A reduction in levels of miR-106b triggers vascular growth both
MeSH term(s)	Animals ; Cell Line ; Cell Movement/genetics ; Choroidal Neovascularization/genetics ; Choroidal Neovascularization/pathology ; Diabetic Retinopathy ; Disease Models, Animal ; Endoplasmic Reticulum Stress/genetics ; Endothelial Cells ; Eye Burns ; Humans ; Laser Therapy ; Macular Degeneration/genetics ; Macular Degeneration/pathology ; Mice ; MicroRNAs/genetics ; Oxygen/toxicity ; Retinal Neovascularization/genetics ; Retinal Neovascularization/pathology ; Retinopathy of Prematurity ; Unfolded Protein Response/genetics ; eIF-2 Kinase/genetics ; eIF-2 Kinase/metabolism
Chemical Substances	MIRN106 microRNA, human ; MicroRNAs ; Mirn106 microRNA, mouse ; PERK kinase (EC 2.7.11.1) ; eIF-2 Kinase (EC 2.7.11.1) ; Oxygen (S88TT14065)
Language	English
Publishing date	2020-12-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.202404
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Article ; Online: Assessment of vascular regeneration in the CNS using the mouse retina.

Miloudi, Khalil / Dejda, Agnieszka / Binet, François / Lapalme, Eric / Cerani, Agustin / Sapieha, Przemyslaw

Journal of visualized experiments : JoVE

2014 , Issue 88, Page(s) e51351

Abstract: The rodent retina is perhaps the most accessible mammalian system in which to investigate neurovascular interplay within the central nervous system (CNS). It is increasingly being recognized that several neurodegenerative diseases such as Alzheimer's, ... ...

Abstract	The rodent retina is perhaps the most accessible mammalian system in which to investigate neurovascular interplay within the central nervous system (CNS). It is increasingly being recognized that several neurodegenerative diseases such as Alzheimer's, multiple sclerosis, and amyotrophic lateral sclerosis present elements of vascular compromise. In addition, the most prominent causes of blindness in pediatric and working age populations (retinopathy of prematurity and diabetic retinopathy, respectively) are characterized by vascular degeneration and failure of physiological vascular regrowth. The aim of this technical paper is to provide a detailed protocol to study CNS vascular regeneration in the retina. The method can be employed to elucidate molecular mechanisms that lead to failure of vascular growth after ischemic injury. In addition, potential therapeutic modalities to accelerate and restore healthy vascular plexuses can be explored. Findings obtained using the described approach may provide therapeutic avenues for ischemic retinopathies such as that of diabetes or prematurity and possibly benefit other vascular disorders of the CNS.
MeSH term(s)	Animals ; Brain Ischemia/physiopathology ; Disease Models, Animal ; Mice ; Neovascularization, Pathologic/physiopathology ; Nerve Regeneration/physiology ; Oxygen ; Retina/drug effects ; Retina/pathology ; Retina/physiopathology ; Retinal Diseases/physiopathology ; Retinal Vessels/pathology
Chemical Substances	Oxygen (S88TT14065)
Language	English
Publishing date	2014-06-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Video-Audio Media
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/51351
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