ArticleMolecular medicine reports2016
Cytoplasmic translocation of high-mobility group box-1 protein is induced by diabetes and high glucose in retinal pericytes.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Protective effects of nattokinase against microvasculopathy and neuroinflammation in diabetic retinopathy.Journal of diabetes · 2023Article
- Contraction of human brain vascular pericytes in response to islet amyloid polypeptide is reversed by pramlintide.Molecular brain · 2023Article
- Role of HMGB1 signaling in the inflammatory process in diabetic retinopathy.Cellular signalling · 2020Review
- The Complex Relationship between Diabetic Retinopathy and High-Mobility Group Box: A Review of Molecular Pathways and Therapeutic Strategies.Antioxidants (Basel, Switzerland) · 2020Review
- Role of Moesin Phosphorylation in Retinal Pericyte Migration and Detachment Induced by Advanced Glycation Endproducts.Frontiers in endocrinology · 2020Article
- High Mobility Group Box-1 and Diabetes Mellitus Complications: State of the Art and Future Perspectives.International journal of molecular sciences · 2019Review
- Glycyrrhizin Protects the Diabetic Retina against Permeability, Neuronal, and Vascular Damage through Anti-Inflammatory Mechanisms.Journal of clinical medicine · 2019Article
- Diminished LINC00173 expression induced miR-182-5p accumulation promotes cell proliferation, migration and apoptosis inhibition via AGER/NF-κB pathway in non-small-cell lung cancer.American journal of translational research · 2019Article
- HMGB1 inhibits insulin signalling through TLR4 and RAGE in human retinal endothelial cells.Growth factors (Chur, Switzerland) · 2018Article
- The Association Between Variants of Receptor for Advanced Glycation End Products (RAGE) Gene Polymorphisms and Age-Related Macular Degeneration.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Sodium Butyrate Ameliorates Streptozotocin-Induced Type 1 Diabetes in Mice by Inhibiting the HMGB1 Expression.Frontiers in endocrinology · 2018Article
- Proinflammatory Effect of High Glucose Concentrations on HMrSV5 Cells via the Autocrine Effect of HMGB1.Frontiers in physiology · 2017Article
- HMGB1 siRNA can reduce damage to retinal cells induced by high glucose in vitro and in vivo.Drug design, development and therapy · 2017Article
- High Mobility Group Box-1: A Missing Link between Diabetes and Its Complications.Mediators of inflammation · 2016Review
- Effects of Glycyrrhizin Treatment on Diabetic Cornea.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and TherapeuticsArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to assess the involvement of the high-mobility group box-1 (HMGB1) protein, receptor for advanced glycation end products (RAGE) and nuclear factor (NF)-κB signaling pathway in the development of diabetic retinopathy. Rat primary retinal pericytes were exposed to 25 mmol/l D‑glucose for 48 h. Diabetic retinal vessels were prepared from streptozotocin-induced diabetic rats 12 weeks following the induction of diabetes. The expression of HMGB1 was detected using immunofluorescence staining. The expression of RAGE and the activity of NF‑κB were analyzed using western blot and electrophoretic mobility shift assays, respectively. The results showed that HMGB1 was translocated to the cytoplasm of the high glucose‑treated pericytes and diabetic retinal pericytes, whereas, in the control cells and the normal retinas, HMGB1 was expressed in the cell nuclei only. The expression of RAGE, a potential receptor for HMGB1, and the activity of NF‑κB were also increased in the high glucose‑treated pericytes, compared with the normal control cells. In addition, high glucose increased the binding of NF‑κB to the RAGE promoter. These findings suggested that the cytoplasmic translocation of HMGB1 may be caused by diabetes and high glucose in retinal pericytes, and that the pathogenic role of HMGB1 may be dependent on the expression of RAGE and activation of NF‑κB.
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