ArticleBMC systems biology2013
Transdifferentiation of pancreatic cells by loss of contact-mediated signaling.
Article in BMC systems biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Recombinant Reg3α Prevents Islet β-Cell Apoptosis and Promotes β-Cell Regeneration.International journal of molecular sciences · 2022Article
- Agent-based modeling and bifurcation analysis reveal mechanisms of macrophage polarization and phenotype pattern distribution.Scientific reports · 2019Article
- Computational Analysis of Altering Cell Fate.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Systematic single-cell analysis provides new insights into heterogeneity and plasticity of the pancreas.Molecular metabolism · 2017Review
- Antidiabetic and Antioxidant Impacts of Desert Date (Balanites aegyptiaca) and Parsley (Petroselinum sativum) Aqueous Extracts: Lessons from Experimental Rats.Journal of diabetes research · 2016Article
- Development, growth and maintenance of β-cell mass: models are also part of the story.Molecular aspects of medicine · 2015Review
- Morpheus: a user-friendly modeling environment for multiscale and multicellular systems biology.Bioinformatics (Oxford, England) · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundReplacement of dysfunctional β-cells in the islets of Langerhans by transdifferentiation of pancreatic acinar cells has been proposed as a regenerative therapy for diabetes. Adult acinar cells spontaneously revert to a multipotent state upon tissue dissociation in vitro and can be stimulated to redifferentiate into β-cells. Despite accumulating evidence that contact-mediated signals are involved, the mechanisms regulating acinar-to-islet cell transdifferentiation remain poorly understood.
resultsIn this study, we propose that the crosstalk between two contact-mediated signaling mechanisms, lateral inhibition and lateral stabilization, controls cell fate stability and transdifferentiation of pancreatic cells. Analysis of a mathematical model combining gene regulation with contact-mediated signaling reveals the multistability of acinar and islet cell fates. Inhibition of one or both modes of signaling results in transdifferentiation from the acinar to the islet cell fate, either by dedifferentiation to a multipotent state or by direct lineage switching.
conclusionsThis study provides a theoretical framework to understand the role of contact-mediated signaling in pancreatic cell fate control that may help to improve acinar-to-islet cell transdifferentiation strategies for β-cell neogenesis.
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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.