ArticleMolecular biology of the cell2016
Virtual-tissue computer simulations define the roles of cell adhesion and proliferation in the onset of kidney cystic disease.
Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Biophysics of lumen morphogenesis.Development (Cambridge, England) · 2026Review
- Adhesion and polarity-driven morphogenesis: Mechanisms and constraints in tissue formation.PLoS computational biology · 2026Article
- Who's afraid of synthetic data? Hybrid approaches to deliver medical digital twins.Informatics in medicine unlocked · 2026Article
- Modeling of viscous frictional force in multicellular morphogenesis.Biophysics and physicobiology · 2026Article
- Apical constriction requires patterned apical surface remodeling to synchronize cellular deformation.eLife · 2025Article
- Article
- Programming the elongation of mammalian cell aggregates with synthetic gene circuits.bioRxiv : the preprint server for biology · 2024Article
- Novel imaging and biophysical approaches to study tissue hydraulics in mammalian folliculogenesis.Biophysical reviews · 2024Review
- Morphological basis of the lung adenocarcinoma subtypes.iScience · 2024Article
- Effective mechanical potential of cell-cell interaction in tissues harboring cavity and in cell sheet toward morphogenesis.Frontiers in cell and developmental biology · 2024Article
- Computational study of biomechanical drivers of renal cystogenesis.Biomechanics and modeling in mechanobiology · 2023Article
- Effective mechanical potential of cell-cell interaction explains three-dimensional morphologies during early embryogenesis.PLoS computational biology · 2023Article
- Article
- Parameterized Computational Framework for the Description and Design of Genetic Circuits of Morphogenesis Based on Contact-Dependent Signaling and Changes in Cell-Cell Adhesion.ACS synthetic biology · 2022Article
- A Negative Feedback Loop and Transcription Factor Cooperation Regulate Zonal Gene Induction by 2, 3, 7, 8-Tetrachlorodibenzo-p-Dioxin in the Mouse Liver.Hepatology communications · 2022Article
- Quantitative modeling identifies critical cell mechanics driving bile duct lumen formation.PLoS computational biology · 2022Article
- Generation of multicellular spatiotemporal models of population dynamics from ordinary differential equations, with applications in viral infection.BMC biology · 2021Article
- A mechanical model of early somite segmentation.iScience · 2021Article
- CompuCell3D Simulations Reproduce Mesenchymal Cell Migration on Flat Substrates.Biophysical journal · 2020Article
- Synthetic development: building mammalian multicellular structures with artificial genetic programs.Current opinion in biotechnology · 2019Review
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8 authors.
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Abstract
In autosomal dominant polycystic kidney disease (ADPKD), cysts accumulate and progressively impair renal function. Mutations in PKD1 and PKD2 genes are causally linked to ADPKD, but how these mutations drive cell behaviors that underlie ADPKD pathogenesis is unknown. Human ADPKD cysts frequently express cadherin-8 (cad8), and expression of cad8 ectopically in vitro suffices to initiate cystogenesis. To explore cell behavioral mechanisms of cad8-driven cyst initiation, we developed a virtual-tissue computer model. Our simulations predicted that either reduced cell-cell adhesion or reduced contact inhibition of proliferation triggers cyst induction. To reproduce the full range of cyst morphologies observed in vivo, changes in both cell adhesion and proliferation are required. However, only loss-of-adhesion simulations produced morphologies matching in vitro cad8-induced cysts. Conversely, the saccular cysts described by others arise predominantly by decreased contact inhibition, that is, increased proliferation. In vitro experiments confirmed that cell-cell adhesion was reduced and proliferation was increased by ectopic cad8 expression. We conclude that adhesion loss due to cadherin type switching in ADPKD suffices to drive cystogenesis. Thus, control of cadherin type switching provides a new target for therapeutic intervention.
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