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Chen, C.-W., Guan, B.-J., & Alzahrani, M. R. (2022). Adaptation to chronic ER stress enforces pancreatic β-cell plasticity. Nature Communications, 13(1), 4621. Added by: Dr. Enrique Feoli (21/02/2024, 13:09) Last edited by: Dr. Enrique Feoli (21/02/2024, 13:12) |
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| Resource type: Journal Article DOI: 10.1038/s41467-022-32425-7 ID no. (ISBN etc.): 2041-1723 BibTeX citation key: Chen2022 View all bibliographic details  |
Categories: BioAcyl Corp Subcategories: Cell plasticity Keywords: , Creators: Alzahrani, Chen, Guan Collection: Nature Communications |
Views: 2/343
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| Abstract |
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Pancreatic β-cells are prone to endoplasmic reticulum (ER) stress due to their role in insulin secretion. They require sustainable and efficient adaptive stress responses to cope with this stress. Whether episodes of chronic stress directly compromise β-cell identity is unknown. We show here under reversible, chronic stress conditions β-cells undergo transcriptional and translational reprogramming associated with impaired expression of regulators of β-cell function and identity. Upon recovery from stress, β-cells regain their identity and function, indicating a high degree of adaptive plasticity. Remarkably, while β-cells show resilience to episodic ER stress, when episodes exceed a threshold, β-cell identity is gradually lost. Single cell RNA-sequencing analysis of islets from type 1 diabetes patients indicates severe deregulation of the chronic stress-adaptation program and reveals novel biomarkers of diabetes progression. Our results suggest β-cell adaptive exhaustion contributes to diabetes pathogenesis.
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| Notes |
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Number: 1 Publisher: Nature Publishing Group
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