{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Paulson SG"],"funding":["U.S. Department of Defense","Cosmos Club Foundation","National Institutes of Health","Uniformed Services University","NIH HHS","NIGMS NIH HHS","Uniformed Services University of the Health Sciences"],"pagination":["bio062021"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12486203"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(9)"],"pubmed_abstract":["Physical confinement is not routinely considered as a factor that influences phagocytosis, which is typically investigated using unconfined in vitro assays. BV2 microglia-like cells were used to interrogate the impact of confinement on IgG-mediated phagocytosis side by side with unconfined cells. Confinement acted as a potent phagocytic driver, greatly increasing the fraction of phagocytic cells in the population compared to the unconfined setting. Arp2/3 complex and myosin II contributed to this effect. Remarkably, confinement partially rescued phagocytic uptake upon myosin II disruption. In addition, cells under confinement were partially resistant to the actin-depolymerizing drug cytochalasin D. Unexpectedly, we observed that bead uptake stimulated persistent migration, a process we ter"],"journal":["Biology open"],"pubmed_title":["Physical confinement and phagocytic uptake induce persistent cell migration."],"pmcid":["PMC12486203"],"funding_grant_id":["HU00012320103","R01 GM134104","Department of Defense","GM134104"],"pubmed_authors":["Liu S","Paulson SG","Rotty JD"],"additional_accession":[]},"is_claimable":false,"name":"Physical confinement and phagocytic uptake induce persistent cell migration.","description":"Physical confinement is not routinely considered as a factor that influences phagocytosis, which is typically investigated using unconfined in vitro assays. BV2 microglia-like cells were used to interrogate the impact of confinement on IgG-mediated phagocytosis side by side with unconfined cells. Confinement acted as a potent phagocytic driver, greatly increasing the fraction of phagocytic cells in the population compared to the unconfined setting. Arp2/3 complex and myosin II contributed to this effect. Remarkably, confinement partially rescued phagocytic uptake upon myosin II disruption. In addition, cells under confinement were partially resistant to the actin-depolymerizing drug cytochalasin D. Unexpectedly, we observed that bead uptake stimulated persistent migration, a process we ter","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-07-15T06:49:23.919Z","creation":"2026-06-30T03:23:51.082Z"},"accession":"S-EPMC12486203","cross_references":{"pubmed":["40888728"],"doi":["10.1242/bio.062021"]}}