ArticleCell & bioscience2012
The protective effect of peroxiredoxin II on oxidative stress induced apoptosis in pancreatic β-cells.
Article in Cell & bioscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 68 citations in OpenAlex.
- Diabetic kidney disease: from pathogenesis to multimodal therapy-current evidence and future directions.Frontiers in medicine · 2025Review
- Characterizing poorly controlled type 2 diabetes usingMetabolomics : Official journal of the Metabolomic Society · 2024Article
- The reprotoxic adverse side effects of neurogenic and neuroprotective drugs: current use of human organoid modeling as a potential alternative to preclinical models.Frontiers in pharmacology · 2024Review
- Reviewing the Prospective Pharmacological Potential of Isothiocyanates in Fight against Female-Specific Cancers.Cancers · 2023Review
- Hydrogen peroxide detoxification through the peroxiredoxin/thioredoxin antioxidant system: A look at the pancreatic β-cell oxidant defense.Vitamins and hormones · 2023Article
- Defining the ferroptotic phenotype of beta cells in type 1 diabetes and its inhibition as a potential antidiabetic strategy.Frontiers in endocrinology · 2023Article
- Redox metabolism correlates with cellular turnover and clinical phenotype of papillary thyroid carcinoma and colloid goiter.Archives of medical science : AMS · 2022Article
- The Role of Thioredoxin/Peroxiredoxin in the β-Cell Defense Against Oxidative Damage.Frontiers in endocrinology · 2021Review
- Single-cell transcriptomics of human islet ontogeny defines the molecular basis of β-cell dedifferentiation in T2D.Molecular metabolism · 2020Article
- Redox-Oligomeric State of Peroxiredoxin-2 and Glyceraldehyde-3-Phosphate Dehydrogenase in Obstructive Sleep Apnea Red Blood Cells under Positive Airway Pressure Therapy.Antioxidants (Basel, Switzerland) · 2020Article
- Peroxiredoxin I deficiency increases pancreatic β‑cell apoptosis after streptozotocin stimulation via the AKT/GSK3β signaling pathway.Molecular medicine reports · 2020Article
- Peroxiredoxin 1 plays a primary role in protecting pancreatic β-cells from hydrogen peroxide and peroxynitrite.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- Contribution of Oxidative Stress and Impaired Biogenesis of Pancreatic β-Cells to Type 2 Diabetes.Antioxidants & redox signaling · 2019Article
- Pancreatic β-cells detoxify HThe Journal of biological chemistry · 2019Article
- Effect of Age on the Protein Profile of Healthy Malay Adults and its Association with Cognitive Function Competency.Journal of Alzheimer's disease : JAD · 2019Article
- Matrix association region/scaffold attachment region (MAR/SAR) sequence: its vital role in mediating chromosome breakages in nasopharyngeal epithelial cells via oxidative stress-induced apoptosis.BMC molecular biology · 2018Article
- Fatty Acid-Stimulated Insulin Secretion vs. Lipotoxicity.Molecules (Basel, Switzerland) · 2018Review
- Mitochondrial Molecular Abnormalities Revealed by Proteomic Analysis of Hippocampal Organelles of Mice Triple Transgenic for Alzheimer Disease.Frontiers in molecular neuroscience · 2018Article
- Hyperglycemia decreases preoxiredoxin-2 expression in a middle cerebral artery occlusion model.Laboratory animal research · 2017Article
- Tracing the dynamics of gene transcripts after organismal death.Open biology · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive loss of pancreatic β-cells, mainly through apoptosis, contributes to the development of diabetic hyperglycemia. Oxidative stress plays a major role in the process of β-cell apoptosis due to low expression level of endogenous antioxidants in the β-cells. Peroxiredoxins (PRDX) are a family of peroxide reductases which uses thioredoxin to clear peroxides. Several members of PRDX have been found in β-cells and recent studies suggested that these antioxidant enzymes possess protective effects in β-cells against oxidative stress mediated apoptosis. In this study, we aimed to investigate the role of PRDX2 in modulating β-cell functions. We detected the expression of PRDX2 both at the transcript and protein levels in the clonal β-cells INS-1 and MIN6 as well as rodent islets. Western blot showed that treatment of MIN6 β-cell line with proinflammatory cytokines, palmitic acid or streptozotocin dose- or time-dependently increased apoptosis, which was associated with reduced endogenous expression levels of PRDX2. To examine the role for PRDX2 in the apoptotic stimuli-induced β-cell apoptosis, we used plasmid overexpression and siRNA knockdown strategies to investigate whether the elevation or knockdown of PRDX2 affects stimuli-induced apoptosis in the β-cells. Remarkably, overexpression of PRDX2 in MIN6 cells significantly attenuated the oxidative stresses mediated apoptosis, as evaluated by cleaved caspase 3 expression, nuclear condensation and fragmentation, as well as FACS analysis. Conversely, attenuation of PRDX2 protein expression using siRNA knockdown exaggerated the cell death induced by proinflammatory cytokines and palmitic acid in the MIN6 cells. These results suggest that PRDX2 may play a protective role in pancreatic β-cells under oxidative stress.
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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.