ArticleExperimental eye research2007
Heterotypic RPE-choroidal endothelial cell contact increases choroidal endothelial cell transmigration via PI 3-kinase and Rac1.
Article in Experimental eye research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- LIF, a mitogen for choroidal endothelial cells, protects the choriocapillaris: implications for prevention of geographic atrophy.EMBO molecular medicine · 2022Article
- Review
- 7-ketocholesterol induces endothelial-mesenchymal transition and promotes fibrosis: implications in neovascular age-related macular degeneration and treatment.Angiogenesis · 2021Article
- Active Rap1-mediated inhibition of choroidal neovascularization requires interactions with IQGAP1 in choroidal endothelial cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- IQGAP1 causes choroidal neovascularization by sustaining VEGFR2-mediated Rac1 activation.Angiogenesis · 2020Article
- Roles of Nicotinamide Adenine Dinucleotide Phosphate (NADPH) Oxidase in Angiogenesis: Isoform-Specific Effects.Antioxidants (Basel, Switzerland) · 2017Review
- Thy-1 Regulates VEGF-Mediated Choroidal Endothelial Cell Activation and Migration: Implications in Neovascular Age-Related Macular Degeneration.Investigative ophthalmology & visual science · 2016Article
- PKR promotes choroidal neovascularization via upregulating the PI3K/Akt signaling pathway in VEGF expression.Molecular vision · 2016Article
- Regulation of signaling events involved in the pathophysiology of neovascular AMD.Molecular vision · 2016Review
- Retinal pigment epithelial cell expression of active Rap 1a by scAAV2 inhibits choroidal neovascularization.Molecular therapy. Methods & clinical development · 2016Article
- Rap1 GTPase Inhibits Tumor Necrosis Factor-α-Induced Choroidal Endothelial Migration via NADPH Oxidase- and NF-κB-Dependent Activation of Rac1.The American journal of pathology · 2015Article
- Ras-related C3 botulinum toxin substrate 1 activation is involved in the pathogenesis of diabetic retinopathy.Experimental and therapeutic medicine · 2015Article
- Activation of Rap1 inhibits NADPH oxidase-dependent ROS generation in retinal pigment epithelium and reduces choroidal neovascularization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Rap1 GTPase activation and barrier enhancement in rpe inhibits choroidal neovascularization in vivo.PloS one · 2013Article
- Upregulation of CCR3 by age-related stresses promotes choroidal endothelial cell migration via VEGF-dependent and -independent signaling.Investigative ophthalmology & visual science · 2011Article
- The small GTPase Rap1 is a novel regulator of RPE cell barrier function.Investigative ophthalmology & visual science · 2011Article
- Influence of Dll4 via HIF-1α-VEGF signaling on the angiogenesis of choroidal neovascularization under hypoxic conditions.PloS one · 2011Article
- Breaking barriers: insight into the pathogenesis of neovascular age-related macular degeneration.Eye and brain · 2011Article
- The role of RPE cell-associated VEGF₁₈₉ in choroidal endothelial cell transmigration across the RPE.Investigative ophthalmology & visual science · 2011Article
- The role of vascular endothelial growth factor-induced activation of NADPH oxidase in choroidal endothelial cells and choroidal neovascularization.The American journal of pathology · 2010Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Age-related macular degeneration (AMD) is the major cause of non-preventable blindness. Severe forms of AMD involve breaching of the retinal pigment epithelial (RPE) barrier by underlying choroidal endothelial cells (CECs), followed by migration into, and subsequent neovascularization of the neurosensory retina. However, little is known about the interactions between RPE and CECs and the signaling events leading to CEC transmigration. While soluble chemotactic factors secreted from RPE can contribute to inappropriate CEC transmigration, other unidentified stimuli may play an additional role. Using a coculture model that maintains the natural structural orientation of CECs to the basal aspect of RPE, we show that "contact" with RPE and/or RPE extracellular matrix increases CEC transmigration of the RPE barrier. From a biochemical standpoint, contact between CECs and RPE results in an increase in the activity of the GTPase Rac1 within the CECs; this increase is dependent on upstream activation of PI 3-K and Akt1. To confirm a link between these signaling molecules and increased CEC transmigration, we performed transmigration assays while inhibiting both PI 3-K and Rac1 activity, and observed that both decreased CEC transmigration. We hypothesize that contact between CECs and RPE stimulates a signaling pathway involving PI 3-K, Akt1, and Rac1 that facilitates CEC transmigration across the RPE barrier, an important step in the development of neovascular AMD.
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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.