ArticleInvestigative ophthalmology & visual science2013
DNA-PK phosphorylation of IGFBP-3 is required to prevent apoptosis in retinal endothelial cells cultured in high glucose.
Article in Investigative ophthalmology & visual science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- PKA prevents the resection of DNA double-strand breaks and favours nonhomologous end-joining.Scientific reports · 2025Article
- Signaling Pathways of the Insulin-like Growth Factor Binding Proteins.Endocrine reviews · 2023Article
- Inhibition of non-homologous end joining of gamma ray-induced DNA double-strand breaks by cAMP signaling in lung cancer cells.Scientific reports · 2020Article
- Protein Kinase Inhibitor Peptide as a Tool to Specifically Inhibit Protein Kinase A.Frontiers in physiology · 2020Review
- IGFBP-3 interacts with NONO and SFPQ in PARP-dependent DNA damage repair in triple-negative breast cancer.Cellular and molecular life sciences : CMLS · 2019Article
- Mutual regulation between IGF-1R and IGFBP-3 in human corneal epithelial cells.Journal of cellular physiology · 2019Article
- PKA regulates HMGB1 through activation of IGFBP-3 and SIRT1 in human retinal endothelial cells cultured in high glucose.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Article
- miR-146a suppresses STAT3/VEGF pathways and reduces apoptosis through IL-6 signaling in primary human retinal microvascular endothelial cells in high glucose conditions.Vision research · 2017Article
- Epac1 agonist decreased inflammatory proteins in retinal endothelial cells, and loss of Epac1 increased inflammatory proteins in the retinal vasculature of mice.Molecular vision · 2017Article
- Compound 49b Regulates ZO-1 and Occludin Levels in Human Retinal Endothelial Cells and in Mouse Retinal Vasculature.Investigative ophthalmology & visual science · 2017Article
- Review
- Effects of antioxidant gene therapy on the development of diabetic retinopathy and the metabolic memory phenomenon.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2015Article
- IGFBP-3 may trigger osteoarthritis by inducing apoptosis of chondrocytes through Nur77 translocation.International journal of clinical and experimental pathology · 2015Article
- Sodium salicylate reduced insulin resistance in the retina of a type 2 diabetic rat model.PloS one · 2015Article
- Pioglitazone restores IGFBP-3 levels through DNA PK in retinal endothelial cells cultured in hyperglycemic conditions.Investigative ophthalmology & visual science · 2014Article
- Article
- IGF binding proteins in cancer: mechanistic and clinical insights.Nature reviews. Cancer · 2014Review
- A sensitive and fast LC-MS/MS method for determination of β-receptor agonist JP-49b: application to a pharmacokinetic study in rats.Journal of chromatography. B, Analytical technologies in the biomedical and life sciences · 2014Article
- TNFα inhibits IGFBP-3 through activation of p38α and casein kinase 2 in human retinal endothelial cells.PloS one · 2014Article
- Intravitreal injection of IGFBP-3 restores normal insulin signaling in diabetic rat retina.PloS one · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
purposeThe goal of this study was to determine whether Compound 49b stimulates insulin-like growth factor binding protein-3 (IGFBP-3) activation in retinal endothelial cells (REC) through DNA-dependent protein kinase (DNA-PK).
methodsREC were grown in a normal glucose (5 mM) or high glucose medium (25 mM). Some cells were transfected with protein kinase A (PKA) siRNA, following treatment with 50 nM Compound 49b, a novel β-adrenergic receptor agonist. Cell proteins were extracted and analyzed for DNA-PK expression by Western blotting. Additional cells were treated with or without NU7441 (a specific DNA-PK inhibitor) prior to Compound 49b treatment. Cell lysates were processed for IGFBP-3 ELISA analyses and Western blotting to measure casein kinase 2 (CK2). Immunoprecipitation for total and phospho-IGFBP-3, cell proliferation and cell death measurements were done after transfection with the S(156)A IGFBP-3 mutation (key phosphorylation site involved in DNA-PK) plasmid DNA.
resultsCompound 49b required DNA-PK to activate IGFBP-3 in REC. IGFBP-3 activation was significantly reduced following treatment with either the DNA-PK inhibitor or following transfection with the IGFBP-3 S(156)A mutant plasmid (P < 0.05). Significant increases in cell death and decreases in cell proliferation were also observed in cells transfected with the IGFBP-3 S(156)A mutant plasmid (P < 0.05). Casein kinase levels were not altered after treatment with NU7741 or Compound 49b.
conclusionsOur findings suggest Compound 49b induces DNA-PK levels through PKA activity. DNA-PK is required for Compound 49b-induced IGFBP-3 expression, leading to inhibition of REC cell death.
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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 OpenQuestion graph.