ArticleCell cycle (Georgetown, Tex.)2014
A genetic mouse model for progressive ablation and regeneration of insulin producing beta-cells.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Moderate beta-cell ablation triggers synergic compensatory mechanisms even in the absence of overt metabolic disruption.Communications biology · 2024Article
- Insulin micro-secretion in Type 1 diabetes and related microRNA profiles.Scientific reports · 2021Article
- A Regeneration Toolkit.Developmental cell · 2018Review
- Regeneration of islet β-cells in tree shrews and rats.Animal models and experimental medicine · 2018Article
- TIF-IA: An oncogenic target of pre-ribosomal RNA synthesis.Biochimica et biophysica acta · 2016Review
- Stress-induced adaptive islet cell identity changes.Diabetes, obesity & metabolism · 2016Review
- Autonomous interconversion between adult pancreatic α-cells and β-cells after differential metabolic challenges.Molecular metabolism · 2016Article
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Authors and funding
4 authors at 4 institutions in 4 countries.
Funding
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Abstract
The putative induction of adult β-cell regeneration represents a promising approach for the treatment of type 1 diabetes. Toward this ultimate goal, it is essential to develop an inducible model mimicking the long-lasting disease progression. In the current study, we have established a novel β-cell ablation mouse model, in which the β-cell mass progressively declines, as seen in type 1 diabetes. The model is based on the β-cell specific genetic ablation of the transcription initiation factor 1A, TIF-IA, essential for RNA Polymerase I activity (TIF-IA(Δ/Δ)). Using this approach, we induced a slow apoptotic response that eventually leads to a protracted β-cell death. In this model, we observed β-cell regeneration that resulted in a complete recovery of the β-cell mass and normoglycemia. In addition, we showed that adaptive proliferation of remaining β-cells is the prominent mechanism acting to compensate for the massive β-cell loss in young but also aged mice. Interestingly, at any age, we also detected β-like cells expressing the glucagon hormone, suggesting a transition between α- and β-cell identities or vice versa. Taken together, the TIF-IA(Δ/Δ) mouse model can be used to investigate the potential therapeutic approaches for type 1 diabetes targeting β-cell regeneration.
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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.