ArticleCell cycle (Georgetown, Tex.)2023
Upregulated miR-194-5p suppresses retinal microvascular endothelial cell dysfunction and mitigates the symptoms of hypertensive retinopathy in mice by targeting SOX17 and VEGF signaling.
Article in Cell cycle (Georgetown, Tex.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- In-depth analysis of retinal RNA transcriptome sequencing in a rat model of hypertensive retinopathy.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Article
- Inhibition of angiogenesis by propranolol in infantile hemangiomas via lncRNA NEAT1-mediated miR-194-5p/TRAF6/NF-κB pathway.Pediatric research · 2026Article
- Circulating microRNAs as Biomarkers of Brain Metastases in Lung Cancer: A Pilot Study.Journal of clinical medicine · 2026Article
- Exploring extracellular vesicle MicroRNAs in Usher syndrome type 1B: Tear-Derived EVs as potential indicators of retinal health.Cellular and molecular life sciences : CMLS · 2026Article
- Therapeutic potential of SOX family transcription factors in osteoarthritis.Annals of medicine · 2025Review
- Integrated proteomics analysis and network pharmacology to elucidate the mechanism of Zhilong Huoxue Tongyu Capsule alleviate hypertensive retinopathy in Ang II infusion mice model.Frontiers in pharmacology · 2025Article
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5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHypertensive retinopathy (HR) is a retinal disease that may lead to vision loss and blindness. Sex-determining region Y (SRY)-box (SOX) family transcription factors have been reported to be involved in HR development. In this study, the role and upstream mechanism of SRY-box transcription factor 17 (SOX17) in HR pathogenesis were investigated.
methodsSOX17 and miR-194-5p levels in Angiotensin II (Ang II)-stimulated human retinal microvascular endothelial cells (HRMECs) and retinas of mice were detected by RT-qPCR. SOX17 protein level as well as levels of tight junction proteins and vascular endothelial growth factor (VEGF) signaling-associated proteins were quantified by western blotting. Tube formation assays were performed to evaluate angiogenesis in HRMECs. The structure of mouse retinal tissues was observed by H&E staining. The interaction between miR-194-5p and SOX17 was confirmed by a luciferase reporter assay.
resultsSOX17 was upregulated in HRMECs treated with Ang II. SOX17 knockdown inhibited angiogenesis in Ang II-stimulated HRMECs and increased tight junction protein levels. Mechanically, SOX17 was targeted by miR-194-5p. Moreover, miR-194-5p upregulation restrained angiogenesis and increased tight junction protein levels in Ang II-treated HRMECs, and the effect was reversed by SOX17 overexpression. MiR-194-5p elevation inactivated VEGF signaling via targeting SOX17. miR-194-5p alleviated pathological symptoms of HR in Ang II-treated mice, and its expression was negatively correlated with SOX17 expression in the retinas of model mice.
conclusionsMiR-194-5p upregulation suppressed Ang II-stimulated HRMEC dysfunction and mitigates the symptoms of HR in mice by regulating the SOX17/VEGF signaling.
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