ArticleBMJ open diabetes research & care2021
RUNX1 can mediate the glucose and O-GlcNAc-driven proliferation and migration of human retinal microvascular endothelial cells.
Article in BMJ open diabetes research & care, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Continuous Suppression of Pathological Retinal and Choroidal Neovascularization in Cynomolgus Monkeys via Noninvasive Ophthalmic Delivery of a Novel Anti-VEGFA Nanobody and Proprietary Penetratin Analog Formulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeted siRNA Delivery Against RUNX1 Via tFNA: Inhibiting Retinal Neovascularization and Restoring Vessels Through Dll4/Notch1 Signaling.Investigative ophthalmology & visual science · 2025Article
- Targeting Runx1 in Pathological Retinal Angiogenesis: A Potential Therapeutic Approach.Investigative ophthalmology & visual science · 2025Article
- The perspective of ceRNA regulation of circadian rhythm on choroidal neovascularization.Scientific reports · 2024Article
- Cell metabolism pathways involved in the pathophysiological changes of diabetic peripheral neuropathy.Neural regeneration research · 2024Review
- RUN(X) out of blood: emerging RUNX1 functions beyond hematopoiesis and links to Down syndrome.Human genomics · 2023Review
- Beyond VEGF: Targeting Inflammation and Other Pathways for Treatment of Retinal Disease.The Journal of pharmacology and experimental therapeutics · 2023Review
- Review
- Genetic Polymorphisms in the 3'-Untranslated Regions ofBiomedicines · 2022Article
- Identification of the Potential Molecular Mechanisms Linking RUNX1 Activity with Nonalcoholic Fatty Liver Disease, by Means of Systems Biology.Biomedicines · 2022Article
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6 authors at 1 institution in 1 country.
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Abstract
introductionThis study aims to determine whether high glucose condition and dynamic O-linked N-acetylglucosamine (O-GlcNAc) modification can promote the proliferation and migration of human retinal microvascular endothelial cells (HRMECs) and whether Runt-related transcription factor 1 (RUNX1) could mediate the glucose and O-GlcNAc-driven proliferation and migration of HRMECs. RESEARCH DESIGN AND
methodsWestern blot analysis was used to detect the O-GlcNAc modification level and RUNX1 level in cells and retina tissues, cell growth was studied by cell counting kit-8 assay, cell proliferation was detected by immunofluorescence staining. Then, cell migration and tube formation were investigated by scratch-wound assay, Transwell assay, and tube-forming assay. The changes of retinal structure were detected by H&E staining. The O-GlcNAc modification of RUNX1 was detected by immunoprecipitation.
resultsHigh glucose increases pan-cellular O-GlcNAc modification and the proliferation and migration of HRMECs. Hence, O-GlcNAc modification is critical for the proliferation and migration of HRMECs. RUNX1 mediates the glucose and O-GlcNAc-driven proliferation and migration in HRMECs. RUNX1 can be modified by O-GlcNAc, and that the modification is enhanced in a high glucose environment.
conclusionsThe present study reveals that high glucose condition directly affects retinal endothelial cells (EC) function, and O-GlcNAc modification is critical for the proliferation and migration of HRMECs, RUNX1 may take part in this mechanism, and maybe the function of RUNX1 is related to its O-GlcNAc modification level, which provides a new perspective for studying the mechanism of RUNX1 in diabetic retinopathy.
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