ArticleDiabetologia2016
Sensitivity profile of the human EndoC-βH1 beta cell line to proinflammatory cytokines.
Article in Diabetologia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 69 citations in OpenAlex.
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- Anti-obesity and hepatoprotective effects of pyridoxal phosphate in rats with metabolic syndrome by raising anti-oxidant potential in both serum and liver tissue, while also decreasing hepatic nuclear factor expression.Iranian journal of basic medical sciences · 2025Article
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- Safeguarding genomic integrity in beta-cells: implications for beta-cell differentiation, growth, and dysfunction.Biochemical Society transactions · 2024Review
- Untangling the genetics of beta cell dysfunction and death in type 1 diabetes.Molecular metabolism · 2024Review
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- Nrf2 modulates the benefits of evening exercise in type 2 diabetes.Sports medicine and health science · 2023Review
- β Cell Stress and Endocrine Function During T1D: What Is Next to Discover?Endocrinology · 2023Article
- Unveiling nanoscale optical signatures of cytokine-induced β-cell dysfunction.Scientific reports · 2023Article
- Hidden chronic metabolic acidosis of diabetes type 2 (CMAD): Clues, causes and consequences.Reviews in endocrine & metabolic disorders · 2023Review
- Mesenchymal Stem Cell in Pancreatic Islet Transplantation.Biomedicines · 2023Review
- Uses of Papaya Leaf and Seaweed Supplementations for Controlling Glucose Homeostasis in Diabetes.International journal of molecular sciences · 2023Review
- Immunometabolism in type 2 diabetes mellitus: tissue-specific interactions.Archives of medical science : AMS · 2023Article
- Characterization of the functional and transcriptomic effects of pro-inflammatory cytokines on human EndoC-βH5 beta cells.Frontiers in endocrinology · 2023Article
- Building an ensemble learning model for gastric cancer cell line classification via rapid raman spectroscopy.Computational and structural biotechnology journal · 2023Article
- Pancreatic Islet Cells Response to IFNγ Relies on Their Spatial Location within an Islet.Cells · 2022Article
- β-cells regeneration by WL15 of cysteine and glycine-rich protein 2 which reduces alloxan induced β-cell dysfunction and oxidative stress through phosphoenolpyruvate carboxykinase and insulin pathway in zebrafish in-vivo larval model.Molecular biology reports · 2022Article
- Perinatal stress exposure induced oxidative stress, metabolism disorder, and reduced GLUT-2 in adult offspring of rats.Hormones (Athens, Greece) · 2022Article
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
aims/hypothesisThe aim of this study was to perform a detailed analysis of cytokine toxicity in the new human EndoC-βH1 beta cell line.
methodsThe expression profile of the antioxidative enzymes in the new human EndoC-βH1 beta cells was characterised and compared with that of primary beta cells in the human pancreas. The effects of proinflammatory cytokines on reactive oxygen species formation, insulin secretory responsiveness and apoptosis of EndoC-βH1 beta cells were determined.
resultsEndoC-βH1 beta cells were sensitive to the toxic action of proinflammatory cytokines. Glucose-dependent stimulation of insulin secretion and an increase in the ATP/ADP ratio was abolished by proinflammatory cytokines without induction of IL-1β expression. Cytokine-mediated caspase-3 activation was accompanied by reactive oxygen species formation and developed more slowly than in rodent beta cells. Cytokines transiently increased the expression of unfolded protein response genes, without inducing endoplasmic reticulum stress-marker genes. Cytokine-mediated NFκB activation was too weak to induce inducible nitric oxide synthase expression. The resultant lack of nitric oxide generation in EndoC-βH1 cells, in contrast to rodent beta cells, makes these cells dependent on exogenously generated nitric oxide, which is released from infiltrating immune cells in human type 1 diabetes, for full expression of proinflammatory cytokine toxicity. CONCLUSIONS/
interpretationEndoC-βH1 beta cells are characterised by an imbalance between H2O2-generating and -inactivating enzymes, and react to cytokine exposure in a similar manner to primary human beta cells. They are a suitable beta cell surrogate for cytokine-toxicity studies.
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