ArticlePloS one2013
Computational models reveal a passive mechanism for cell migration in the crypt.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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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Who cites it
29 citing papers in PubMed, 61 citations in OpenAlex.
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- Emergent Stable Tissue Shapes from the Regulatory Feedback between Morphogens and Cell Growth.bioRxiv : the preprint server for biology · 2025Article
- The ECM and tissue architecture are major determinants of early invasion mediated by E-cadherin dysfunction.Communications biology · 2023Article
- ChemChaste: Simulating spatially inhomogeneous biochemical reaction-diffusion systems for modeling cell-environment feedbacks.GigaScience · 2022Article
- Intestinal villus structure contributes to even shedding of epithelial cells.Biophysical journal · 2021Article
- Modelling the effect of subcellular mutations on the migration of cells in the colorectal crypt.BMC bioinformatics · 2020Article
- Evolution of cooperation in an epithelium.Journal of the Royal Society, Interface · 2019Article
- Antrodin C, an NADPH Dependent Metabolism, Encourages Crosstalk between Autophagy and Apoptosis in Lung Carcinoma Cells by Use of an AMPK Inhibition-Independent Blockade of the Akt/mTOR Pathway.Molecules (Basel, Switzerland) · 2019Article
- Regulators of Intestinal Epithelial Migration in Sepsis.Shock (Augusta, Ga.) · 2019Article
- Asymmetric cell division-dominant neutral drift model for normal intestinal stem cell homeostasis.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- Truncated Adenomatous Polyposis Coli Mutation Induces Asef-Activated Golgi Fragmentation.Molecular and cellular biology · 2018Article
- Chronic TNFα-driven injury delays cell migration to villi in the intestinal epithelium.Journal of the Royal Society, Interface · 2018Article
- Host-microbe interaction in the gastrointestinal tract.Environmental microbiology · 2018Review
- Towards personalized computational oncology: from spatial models of tumour spheroids, to organoids, to tissues.Journal of the Royal Society, Interface · 2018Review
- Interkinetic nuclear migration and basal tethering facilitates post-mitotic daughter separation in intestinal organoids.Journal of cell science · 2017Article
- A hierarchical Bayesian model for understanding the spatiotemporal dynamics of the intestinal epithelium.PLoS computational biology · 2017Article
- Comparing individual-based approaches to modelling the self-organization of multicellular tissues.PLoS computational biology · 2017Article
- Cell proliferation within small intestinal crypts is the principal driving force for cell migration on villi.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Enabling Anyone to Translate Clinically Relevant Ideas to Therapies.Pharmaceutical research · 2017Article
- Deciphering the Complex Signaling Systems That Regulate Intestinal Epithelial Cell Death Processes and Shedding.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Cell migration in the intestinal crypt is essential for the regular renewal of the epithelium, and the continued upward movement of cells is a key characteristic of healthy crypt dynamics. However, the driving force behind this migration is unknown. Possibilities include mitotic pressure, active movement driven by motility cues, or negative pressure arising from cell loss at the crypt collar. It is possible that a combination of factors together coordinate migration. Here, three different computational models are used to provide insight into the mechanisms that underpin cell movement in the crypt, by examining the consequence of eliminating cell division on cell movement. Computational simulations agree with existing experimental results, confirming that migration can continue in the absence of mitosis. Importantly, however, simulations allow us to infer mechanisms that are sufficient to generate cell movement, which is not possible through experimental observation alone. The results produced by the three models agree and suggest that cell loss due to apoptosis and extrusion at the crypt collar relieves cell compression below, allowing cells to expand and move upwards. This finding suggests that future experiments should focus on the role of apoptosis and cell extrusion in controlling cell migration in the crypt.
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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.