ArticleMolecular biology reports2013
High glucose induces mitochondrial p53 phosphorylation by p38 MAPK in pancreatic RINm5F cells.
Article in Molecular biology reports, 2013. 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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15 citing papers in PubMed, 32 citations in OpenAlex.
- The Progression of Cardiac Damage in the Offspring of Mothers with Gestational Diabetes Is Regulated by the p53/miR-34/SIRT1/7 Pathway.International journal of molecular sciences · 2026Article
- The interplay of tumor suppressor p53 and oxidative stress in pancreatic β-cell apoptosis and insulin resistance in newly diagnosed type 2 diabetes mellitus.Diabetology & metabolic syndrome · 2025Article
- Pancreatic β-Cell Apoptosis in Normoglycemic Rats is Due to Mitochondrial Translocation of p53-Induced by the Consumption of Sugar-Sweetened Beverages.Cell biochemistry and biophysics · 2023Article
- Molecular Mechanisms of Apoptosis Induction and Its Regulation by Fatty Acids in Pancreatic β-Cells.International journal of molecular sciences · 2021Review
- Sodium pentobarbital dosages for exsanguination affect biochemical, molecular and histological measurements in rats.Scientific reports · 2020Article
- Article
- Effect of High Glucose-Induced Oxidative Stress on Paraoxonase 2 Expression and Activity in Caco-2 Cells.Cells · 2019Article
- Stretching magnitude-dependent inactivation of AKT by ROS led to enhanced p53 mitochondrial translocation and myoblast apoptosis.Molecular biology of the cell · 2019Article
- Serine 392 phosphorylation modulates p53 mitochondrial translocation and transcription-independent apoptosis.Cell death and differentiation · 2018Article
- Is p53 Involved in Tissue-Specific Insulin Resistance Formation?Oxidative medicine and cellular longevity · 2017Review
- High glucose and insulin enhance uPA expression, ROS formation and invasiveness in breast cancer-derived cells.Cellular oncology (Dordrecht, Netherlands) · 2016Article
- Hyperglycemia promotes p53-Mdm2 interaction but reduces p53 ubiquitination in RINm5F cells.Molecular and cellular biochemistry · 2015Article
- Phagocyte-like NADPH oxidase (Nox2) promotes activation of p38MAPK in pancreatic β-cells under glucotoxic conditions: Evidence for a requisite role of Ras-related C3 botulinum toxin substrate 1 (Rac1).Biochemical pharmacology · 2015Article
- Oxidative Stress Type Influences the Properties of Antioxidants Containing Polyphenols in RINm5F Beta Cells.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Bioinformatics study of cancer-related mutations within p53 phosphorylation site motifs.International journal of molecular sciences · 2014Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic β-cell death in type 2 diabetes has been related to p53 subcellular localisation and phosphorylation. However, the mechanisms by which p53 is phosphorylated and its activation in response to oxidative stress remain poorly understood. Therefore, the aim of this study was to investigate mitochondrial p53 phosphorylation, its subcellular localisation and its relationship with apoptotic induction in RINm5F cells cultured under high glucose conditions. Our results show that p53 phosphorylation in the mitochondrial fraction was greater at ser392 than at ser15. This increased phosphorylation correlated with an increase in reactive oxygen species, a decrease in the Bcl-2/Bax ratio, a release of cytochrome c and an increase in the rate of apoptosis. We also observed a decline in ERK 1/2 phosphorylation over time, which is an indicator of cell proliferation. To identify the kinase responsible for phosphorylating p53, p38 mitogen-activated protein kinase (MAPK) activation was analysed. We found that high glucose induced an increase in p38 MAPK phosphorylation in the mitochondria after 24-72 h. Moreover, the phosphorylation of p53 (ser392) by p38 MAPK in mitochondria was confirmed by colocalisation studies with confocal microscopy. The addition of a specific p38 MAPK inhibitor (SB203580) to the culture medium during high glucose treatment blocked p53 mobilisation to the mitochondria and phosphorylation; thus, the release of cytochrome c and the apoptosis rate in RINm5F cells decreased. These results suggest that mitochondrial p53 phosphorylation by p38 MAPK plays an important role in RINm5F cell death under high glucose conditions.
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