ArticleInternational journal of molecular sciences2022
Role of Autotaxin in High Glucose-Induced Human ARPE-19 Cells.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Evidence Supporting Autotaxin as a Potential New Drug Treatment Target in Patients With Advanced Diabetic Retinopathy.Investigative ophthalmology & visual science · 2025Article
- SMAD specific E3 ubiquitin protein ligase 1 accelerates diabetic macular edema progression by WNT inhibitory factor 1.World journal of diabetes · 2025Article
- Correlation between serum autotaxin levels and optic neuropathy in early diabetic retinopathy: a case-control study.Frontiers in medicine · 2025Article
- Calpain-2 Facilitates Autophagic/Lysosomal Defects and Apoptosis in ARPE-19 Cells and Rats Induced by Exosomes from RPE Cells under NaIOOxidative medicine and cellular longevity · 2023Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Autotaxin (ATX) is an enzymatic with lysophospholipase D (lysoPLD) activity. We investigated the role of ATX in high glucose (HG)-induced human retinal pigment epithelial (ARPE-19) cells to explore the pathogenesis of diabetic retinopathy (DR). We performed a quantitative real-time polymerase chain reaction, Western blotting, immunocytochemistry, enzyme-linked immunosorbent assay, cell permeability assay, and transepithelial electrical resistance measurement in HG-induced ARPE-19 cells and compared their results with those of normal glucose and osmotic pressure controls. ATX expression and its lysoPLD activity, barrier function, and expression of vascular endothelial growth factor receptors VEGFR-1 and VEGFR-2 were downregulated, while fibrotic responses, cytoskeletal reorganization, and transforming growth factor-β expression were upregulated, in the HG group. Our results suggest that HG induces intracellular ATX downregulation, barrier dysfunction, and fibrosis, which are involved in early DR and can be targeted for DR treatment.
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Registered trials
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