ArticleJournal of Zhejiang University. Science. B
Comparative transcriptomic analysis reveals adriamycin-induced apoptosis via p53 signaling pathway in retinal pigment epithelial cells.
Article in Journal of Zhejiang University. Science. B. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Low-level red light inhibits human retinal pigment epithelial cell fibrosis via UBE2C in a myopia-simulating hypoxic microenvironment.European journal of medical research · 2025Article
- miR-92b-3p protects retinal tissues against DNA damage and apoptosis by targeting BTG2 in experimental myopia.Journal of translational medicine · 2024Article
- Enhanced cisplatin chemotherapy sensitivity by self-assembled nanoparticles with Olaparib.Frontiers in bioengineering and biotechnology · 2024Article
- miR-656-3p inhibits melanomas in vitro and in vivo by inducing senescence via inhibiting LMNB2.Journal of cancer research and clinical oncology · 2023Article
- Carvacrol protects the ARPE19 retinal pigment epithelial cells against high glucose-induced oxidative stress, apoptosis, and inflammation by suppressing the TRPM2 channel signaling pathways.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2022Article
- Article
- A Novel Role of IL13Rα2 in the Pathogenesis of Proliferative Vitreoretinopathy.Frontiers in medicine · 2022Article
- Diagnostic value of optic disc retinal nerve fiber layer thickness for diabetic peripheral neuropathy.Journal of Zhejiang University. Science. BArticle
- Identification of PTPRR and JAG1 as key genes in castration-resistant prostate cancer by integrated bioinformatics methodsJournal of Zhejiang University. Science. BArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis paper applied a transcriptomic approach to investigate the mechanisms of adriamycin (ADR) in treating proliferative vitreoretinopathy (PVR) using ARPE-19 cells.
methodsThe growth inhibitory effects of ADR on ARPE-19 cells were assessed by sulforhodamine B (SRB) assay and propidium iodide (PI) staining using flow cytometry. The differentially expressed genes between ADR-treated ARPE-19 cells and normal ARPE-19 cells and the signaling pathways involved were investigated by microarray analysis. Mitochondrial function was detected by JC-1 staining using flow cytometry and the Bcl-2/Bax protein family. The phosphorylated histone H2AX (γ-H2AX), phosphorylated checkpoint kinase 1 (p-CHK1), and phosphorylated checkpoint kinase 2 (p-CHK2) were assessed to detect DNA damage and repair.
resultsADR could significantly inhibit ARPE-19 cell proliferation and induce caspase-dependent apoptosis in vitro. In total, 4479 differentially expressed genes were found, and gene ontology items and the p53 signaling pathway were enriched. A protein-protein interaction analysis indicated that the TP53 protein molecules regulated by ADR were related to DNA damage and oxidative stress. ADR reduced mitochondrial membrane potential and the Bcl-2/Bax ratio. p53-knockdown restored the activation of c-caspase-3 activity induced by ADR by regulating Bax expression, and it inhibited ADR-induced ARPE-19 cell apoptosis. Finally, the levels of the γ-H2AX, p-CHK1, and p-CHK2 proteins were up-regulated after ADR exposure.
conclusionsThe mechanism of ARPE-19 cell death induced by ADR may be caspase-dependent apoptosis, and it may be regulated by the p53-dependent mitochondrial dysfunction, activating the p53 signaling pathway through DNA damage.
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