ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Defective retinal vascular endothelial cell development as a consequence of impaired integrin αVβ8-mediated activation of transforming growth factor-β.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 48 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
48 citing papers in PubMed, 84 citations in OpenAlex.
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- GenX induces offspring vascular endothelial ferroptosis by targeting GPX4 for ubiquitination-dependent degradation.Current research in toxicology · 2025Article
- Microvascular smooth muscle cells exhibit divergent phenotypic switching responses to platelet-derived growth factor and insulin-like growth factor 1.Microvascular research · 2024Article
- Crosstalk between Blood Vessels and Glia during the Central Nervous System Development.Life (Basel, Switzerland) · 2022Review
- Paradoxical role of β8 integrin on angiogenesis and vasculogenic mimicry in glioblastoma.Cell death & disease · 2022Article
- The β8 integrin cytoplasmic domain activates extracellular matrix adhesion to promote brain neurovascular development.Development (Cambridge, England) · 2022Article
- TGFβ: Signaling Blockade for Cancer Immunotherapy.Annual review of cancer biology · 2022Article
- Specialized endothelial tip cells guide neuroretina vascularization and blood-retina-barrier formation.Developmental cell · 2021Article
- TGFβ biology in cancer progression and immunotherapy.Nature reviews. Clinical oncology · 2021Review
- αvβ8 integrin adhesion and signaling pathways in development, physiology and disease.Journal of cell science · 2020Review
- Neuronal and glial regulation of CNS angiogenesis and barriergenesis.Development (Cambridge, England) · 2020Review
- Role ofInternational journal of ophthalmology · 2020Article
- Disruption of the Extracellular Matrix Progressively Impairs Central Nervous System Vascular Maturation Downstream of β-Catenin Signaling.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Wnt Signaling in vascular eye diseases.Progress in retinal and eye research · 2019Review
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Deletions of the genes encoding the integrin αVβ8 (Itgav, Itgb8) have been shown to result in abnormal vascular development in the CNS, including prenatal and perinatal hemorrhage. Other work has indicated that a major function of this integrin in vivo is to promote TGFβ activation. In this paper, we show that Itgb8 mRNA is strongly expressed in murine Müller glia and retinal ganglion cells, but not astrocytes. We further show that Itgb8 deletion in the entire retina severely perturbs development of the murine retinal vasculature, elevating vascular branch point density and vascular coverage in the superficial vascular plexus, while severely impairing formation of the deep vascular plexus. The stability of the mutant vasculature is also impaired as assessed by the presence of hemorrhage and vascular basal lamina sleeves lacking endothelial cells. Specific deletion of Itgb8 in Müller glia and neurons, but not deletion in astrocytes, recapitulates the phenotype observed following Itgb8 in the entire retina. Consistent with αVβ8's role in TGFβ1 activation, we show that retinal deletion of Tgfb1 results in very similar retinal vascular abnormalities. The vascular deficits appear to reflect impaired TGFβ signaling in vascular endothelial cells because retinal deletion of Itgb8 reduces phospho-SMAD3 in endothelial cells and endothelial cell-specific deletion of the TGFβRII gene recapitulates the major deficits observed in the Itgb8 and TGFβ1 mutants. Of special interest, the retinal vascular phenotypes observed in each mutant are remarkably similar to those of others following inhibition of neuropilin-1, a receptor previously implicated in TGFβ activation and signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.