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A cell can bind to itself and form a self-adhesion that can be engineered and harnessed as a new way to adhere cells to engineered materials-a key challenge for biomaterials are demonstrated. Here, a 3D structure smaller is developed than a single cell, that a Self-Adhesion-Tunnel (SAT) is called, that causes cells to wrap around it and bind to themselves. This process is driven through the cadherin proteins that regulate cell-cell adhesion, and it is shown that many of the key elements of a normal cell-cell adhesion are found in self-adhesions. Size and shape of the SAT determine the efficiency of self-adhesion formation, and >90% efficient formation of self-adhesions are observed in both kidney and skin cells per SAT. Self-adhesions can persist for at least 24 hrs and act to stabilize the cell-material interface and reduce migration. Overall, this ability to co-opt the native cell-cell adhesion machinery in cells and use it as an attachment strategy can provide new approaches for soft-tissue implant integration and tissue engineering scaffolds where stable tissue-material interfaces are critical.
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http://dx.doi.org/10.1002/adma.202502425 | DOI Listing |
Dev Growth Differ
September 2025
Laboratory for Epithelial Morphogenesis, RIKEN Center for Biosystems Dynamics Research, Kobe, Japan.
Multicellular organisms generate organizational complexity through morphogenesis, in which mechanical forces orchestrate the movements and deformations of cells and tissues, while chemical signals regulate the molecular events that generate and coordinate these forces. One common denominator that is critical both for mechanics and biochemistry is material property. Material properties define how materials deform or rearrange under applied forces, and how rapidly molecules interact or spread in space and time.
View Article and Find Full Text PDFPRX Life
February 2025
Department of Physics & Astronomy, Johns Hopkins University, Baltimore, Maryland 21218, USA.
When cells in a primary tumor work together to invade into nearby tissue, this can lead to cell dissociations-cancer cells breaking off from the invading front-leading to metastasis. What controls the dissociation of cells and whether they break off singly or in small groups? Can this be determined by cell-cell adhesion or chemotactic cues given to cells? We develop a physical model for this question, based on experiments that mimic aspects of cancer cell invasion using microfluidic devices with microchannels of different widths. Experimentally, most dissociation events ("ruptures") involve single cells breaking off, but we observe some ruptures of large groups (~20 cells) in wider channels.
View Article and Find Full Text PDFEnviron Int
September 2025
Division of Gastrointestinal and Liver Diseases, Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States. Electronic address:
Background: Although per- and polyfluoroalkyl substances (PFAS) have been linked to chronic liver diseases, the specific cellular and molecular mechanisms by which different PFAS contribute to human liver dysfunction remain unclear. This study aims to elucidate those mechanisms.
Methods: We exposed a multi-donor human liver spheroid model composed of multiple cell types to 20 µM of PFHxS, PFOA, PFOS, or PFNA for seven days, followed by single-cell RNA sequencing and lipid staining.
Rev Sci Instrum
September 2025
Leiden Institute of Physics, Leiden University, 2333CC Leiden, The Netherlands.
Whether at the molecular or cellular scale in organisms, cell-cell adhesion adapts to external mechanical cues arising from the static environment of cells and from dynamic interactions between neighboring cells. Cell-cell adhesion needs to resist detachment forces to secure the integrity and internal organization of organisms. In the past, various techniques have been developed to characterize adhesion properties of molecules and cells in vitro and to understand how cells sense and probe their environment.
View Article and Find Full Text PDFJ Cell Sci
September 2025
Department of Biochemistry, University of Illinois at Urbana-Champaign, IL, USA.
We present evidence that the association of Epithelial (E)-cadherin (CHD1) extracellular domain and epidermal growth factor receptor (EGFR, ErbB1) is obligatory for cadherin force transduction signaling. E-cadherin and EGFR associate at cell surfaces, independent of their cytoplasmic domains, and tension on E-cadherin activates EGFR signaling. Using engineered cadherin mutants that disrupt co-immunoprecipitation with EGFR, but not adhesion, we show that the hetero-receptor complex is required to mechanically activate signaling and downstream cytoskeletal remodeling at cadherin adhesions.
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