ArticleInvestigative ophthalmology & visual science2025
Endothelial-Pericyte Interactions Regulate Angiogenesis Via VEGFR2 Signaling During Retinal Development and Disease.
Article in Investigative ophthalmology & visual science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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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Who cites it
5 citing papers in PubMed.
- Endothelial Cell-Pericyte Crosstalk in the Brain Balances Microvascular Stability and Plasticity.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Derivation of functional retinal endothelial cells from human pluripotent stem cells for therapeutics and modelling.Nature biomedical engineering · 2026Article
- Angiogenic Gene Therapy for Lower Extremity Ischemia: Experimental Advances and Clinical Experience.Cells · 2026Review
- Regenerative Approach for Improving Flap Survival: Perspective of Angiogenesis.Biomimetics (Basel, Switzerland) · 2026Review
- Endothelial Klf9 fine-tunes Akt signaling to act as a transcriptional brake restraining retinal angiogenesis.International journal of biological sciences · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Purpose: Endothelial-pericyte interaction disruption causes vascular dropout and pathological angiogenesis, severely impacting visual function in ocular microvascular diseases. This study examines VEGF receptor 2 (VEGFR2) signaling in endothelial-pericyte interactions, highlighting VEGFR2 as a potential therapeutic target for promoting pericyte coverage and decreasing vascular leakage in diseased retinas. Method: Cell-cell interactions with VEGFR2 signaling were assessed using isogenic endothelial cells and pericytes from induced pluripotent stem cells. We investigated changes in VEGFR2 signaling resulting from endothelial-pericyte interactions using quantitative Reverse Transcription PCR, western blot analysis, immunofluorescence staining, migration assays, permeability assays, transendothelial electrical resistance measurements, flow cytometry, and three-dimensional collagen gel vascular networks. We validated VEGFR2 as a therapeutic target via intravitreal injection in the oxygen-induced retinopathy mouse model. Treatment effects were evaluated using western blot analysis, immunofluorescence staining, and an FITC-dextran permeability assay to assess protein expression, pericyte recruitment, and retinal vascular function in response to VEGFR2 modulation. Results: We demonstrate that direct endothelial-pericyte contact, mediated by N-cadherin, downregulates phosphorylated VEGFR2 in endothelial cells, thereby enhancing pericyte migration and promoting endothelial cell barrier function. Intravitreal injection of a VEGFR2 inhibitor in mouse models of the developing retina and oxygen-induced retinopathy increased pericyte recruitment and decreased vascular leakage. The VEGFR2 inhibitor further rescued ischemic retinopathy by enhancing vascularization and tissue growth. Conclusions: Our findings uncover a novel mechanism by which VEGFR2 signaling is regulated through endothelial-pericyte interactions, promoting pericyte migration and strengthening endothelial barrier function. These results suggest a pathway that could be harnessed to support the growth of functional and mature microvasculature in ocular microvascular diseases and tissue regeneration overall.
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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 Socratic graph.