ArticlePloS one2011
Pancreatic β-cell death in response to pro-inflammatory cytokines is distinct from genuine apoptosis.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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Who cites it
45 citing papers in PubMed, 78 citations in OpenAlex.
- Role of SIRT3 in the regulation of Gadd45α expression and DNA repair in β-cells.The Journal of biological chemistry · 2025Article
- RISING STARS: Evidence for established and emerging forms of β-cell death.The Journal of endocrinology · 2024Review
- β-Cell-selective regulation of gene expression by nitric oxide.American journal of physiology. Regulatory, integrative and comparative physiology · 2024Article
- Role of cytosolic and endoplasmic reticulum CaPflugers Archiv : European journal of physiology · 2024Review
- Mitochondrial bioenergetics, metabolism, and beyond in pancreatic β-cells and diabetes.Frontiers in molecular biosciences · 2024Review
- Protective Effects of Hemp (Molecules (Basel, Switzerland) · 2023Article
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- Nephropathic Cystinosis: Pathogenic Roles of Inflammation and Potential for New Therapies.Cells · 2022Review
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- β-Cell Death in Diabetes: Past Discoveries, Present Understanding, and Potential Future Advances.Metabolites · 2021Review
- α-CGRP disrupts amylin fibrillization and regulates insulin secretion: implications on diabetes and migraine.Chemical science · 2021Article
- Partners in Crime: Beta-Cells and Autoimmune Responses Complicit in Type 1 Diabetes Pathogenesis.Frontiers in immunology · 2021Review
- Inhibition of mitochondrial oxidative metabolism attenuates EMCV replication and protects β-cells from virally mediated lysis.The Journal of biological chemistry · 2020Article
- A novel Cre-enabled tetracycline-inducible transgenic system for tissue-specific cytokine expression in the zebrafish: CETI-PIC3.Disease models & mechanisms · 2020Article
- Probiotic mediated NF-κB regulation for prospective management of type 2 diabetes.Molecular biology reports · 2020Review
- Herbal medicine in the treatment of patients with type 2 diabetes mellitus.Chinese medical journal · 2019Review
- Pancreatic deletion of the interleukin-1 receptor disrupts whole body glucose homeostasis and promotes islet β-cell de-differentiation.Molecular metabolism · 2018Article
- Probing the Effect of Physiological Concentrations of IL-6 on Insulin Secretion by INS-1 832/3 Insulinoma Cells under Diabetic-Like Conditions.International journal of molecular sciences · 2018Article
- Article
- Radiation-induced inflammation and autoimmune diseases.Military Medical Research · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A reduction in functional β-cell mass leads to both major forms of diabetes; pro-inflammatory cytokines, such as interleukin-1beta (IL-1β) and gamma-interferon (γ-IFN), activate signaling pathways that direct pancreatic β-cell death and dysfunction. However, the molecular mechanism of β-cell death in this context is not well understood. In this report, we tested the hypothesis that individual cellular death pathways display characteristic phenotypes that allow them to be distinguished by the precise biochemical and metabolic responses that occur during stimulus-specific initiation. Using 832/13 and INS-1E rat insulinoma cells and isolated rat islets, we provide evidence that apoptosis is unlikely to be the primary pathway underlying β-cell death in response to IL-1β+γ-IFN. This conclusion was reached via the experimental results of several different interdisciplinary strategies, which included: 1) tandem mass spectrometry to delineate the metabolic differences between IL-1β+γ-IFN exposure versus apoptotic induction by camptothecin and 2) pharmacological and molecular interference with either NF-κB activity or apoptosome formation. These approaches provided clear distinctions in cell death pathways initiated by pro-inflammatory cytokines and bona fide inducers of apoptosis. Collectively, the results reported herein demonstrate that pancreatic β-cells undergo apoptosis in response to camptothecin or staurosporine, but not pro-inflammatory cytokines.
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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.