ArticlePloS one2011
Role of the mitochondria in immune-mediated apoptotic death of the human pancreatic β cell line βLox5.
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 19 papers.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- Type 1 diabetesNPJ autoimmunity · 2026Article
- Mitochondrial bioenergetics, metabolism, and beyond in pancreatic β-cells and diabetes.Frontiers in molecular biosciences · 2024Review
- Modeling cell-mediated immunity in human type 1 diabetes by engineering autoreactive CD8Frontiers in immunology · 2023Article
- Endoplasmic Reticulum-Mitochondria Crosstalk and Beta-Cell Destruction in Type 1 Diabetes.Frontiers in immunology · 2021Review
- Hormonal dysfunction in adult patients affected with inherited metabolic disorders.Journal of mother and child · 2020Review
- Innate inflammation drives NK cell activation to impair Treg activity.Journal of autoimmunity · 2020Article
- Mitochondrial Reactive Oxygen Species and Type 1 Diabetes.Antioxidants & redox signaling · 2018Review
- Type 1 Interferons Potentiate Human CD8Diabetes · 2017Article
- Inflammatory stress of pancreatic beta cells drives release of extracellular heat-shock protein 90α.Immunology · 2017Article
- Endocrine Dysfunctions in Patients with Inherited Metabolic Diseases.Journal of clinical research in pediatric endocrinology · 2016Article
- Article
- STAT1-mediated down-regulation of Bcl-2 expression is involved in IFN-γ/TNF-α-induced apoptosis in NIT-1 cells.PloS one · 2015Article
- In search of a surrogate: engineering human beta cell lines for therapy.Trends in endocrinology and metabolism: TEM · 2014Article
- Genetics of new-onset diabetes after transplantation.Journal of the American Society of Nephrology : JASN · 2014Article
- Cathepsin B contributes to autophagy-related 7 (Atg7)-induced nod-like receptor 3 (NLRP3)-dependent proinflammatory response and aggravates lipotoxicity in rat insulinoma cell line.The Journal of biological chemistry · 2013Article
- The role of reactive oxygen species and proinflammatory cytokines in type 1 diabetes pathogenesis.Annals of the New York Academy of Sciences · 2013Review
- Immune-mediated β-cell death in type 1 diabetes: lessons from human β-cell lines.European journal of clinical investigation · 2012Review
- Endocrine manifestations related to inherited metabolic diseases in adults.Orphanet journal of rare diseases · 2012Review
- Comparative genetics: synergizing human and NOD mouse studies for identifying genetic causation of type 1 diabetes.The review of diabetic studies : RDS · 2012Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Mitochondria are indispensable in the life and death of many types of eukaryotic cells. In pancreatic beta cells, mitochondria play an essential role in the secretion of insulin, a hormone that regulates blood glucose levels. Unregulated blood glucose is a hallmark symptom of diabetes. The onset of Type 1 diabetes is preceded by autoimmune-mediated destruction of beta cells. However, the exact role of mitochondria has not been assessed in beta cell death. In this study, we examine the role of mitochondria in both Fas- and proinflammatory cytokine-mediated destruction of the human beta cell line, βLox5. IFNγ primed βLox5 cells for apoptosis by elevating cell surface Fas. Consequently, βLox5 cells were killed by caspase-dependent apoptosis by agonistic activation of Fas, but only after priming with IFNγ. This beta cell line undergoes both apoptotic and necrotic cell death after incubation with the combination of the proinflammatory cytokines IFNγ and TNFα. Additionally, both caspase-dependent and -independent mechanisms that require proper mitochondrial function are involved. Mitochondrial contributions to βLox5 cell death were analyzed using mitochondrial DNA (mtDNA) depleted βLox5 cells, or βLox5 ρ(0) cells. βLox5 ρ(0) cells are not sensitive to IFNγ and TNFα killing, indicating a direct role for the mitochondria in cytokine-induced cell death of the parental cell line. However, βLox5 ρ(0) cells are susceptible to Fas killing, implicating caspase-dependent extrinsic apoptotic death is the mechanism by which these human beta cells die after Fas ligation. These data support the hypothesis that immune mediators kill βLox5 cells by both mitochondrial-dependent intrinsic and caspase-dependent extrinsic pathways.
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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.