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Cell migration is a fundamental process for life and is highly dependent on the dynamical and mechanical properties of the cytoskeleton. Intensive physical and biochemical crosstalk among actin, microtubules, and intermediate filaments ensures their coordination to facilitate and enable migration. In this review, we discuss the different mechanical aspects that govern cell migration and provide, for each mechanical aspect, a novel perspective by juxtaposing two complementary approaches to the biophysical study of cytoskeletal crosstalk: live-cell studies (often referred to as top-down studies) and cell-free studies (often referred to as bottom-up studies). We summarize the main findings from both experimental approaches, and we provide our perspective on bridging the two perspectives to address the open questions of how cytoskeletal crosstalk governs cell migration and makes cells move.
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http://dx.doi.org/10.1063/5.0198119 | DOI Listing |
Biology (Basel)
August 2025
School of Marine and Biological Engineering, Yancheng Teachers University, Yancheng 224007, China.
Tensins (TNS1-4) are pivotal molecular scaffolds bridging the actin cytoskeleton to integrin-based adhesions, orchestrating signal transduction and governing cellular processes in cancer. Structurally, the N-terminal actin-binding domain (ABD) in TNS1-3 enables cytoskeletal regulation and interactions with regulators like the Rho GAP DLC1, while ABD-deficient TNS4 functions as a focal adhesion signal amplifier. Functionally, TNS1-3 exhibit context-dependent duality as tumor promoters or suppressors, dictated by tissue-specific microenvironments and signaling crosstalk.
View Article and Find Full Text PDFBiology (Basel)
August 2025
Department of Oral Biology, The Dental College of Georgia, Augusta University, Augusta, GA 30912, USA.
The retina is highly sensitive to oxygen and blood supply, and hypoxia plays a key role in retinal diseases such as diabetic retinopathy (DR) and age-related macular degeneration (AMD). Müller glial cells, which are essential for retinal homeostasis, respond to injury and hypoxia with reactive gliosis, characterized by the upregulation of the glial fibrillary acidic protein (GFAP) and vimentin, cellular hypertrophy, and extracellular matrix changes, which can impair retinal function and repair. The retinal pigment epithelium (RPE) supports photoreceptors, forms part of the blood-retinal barrier, and protects against oxidative stress; its dysfunction contributes to retinal degenerative diseases such as AMD, retinitis pigmentosa (RP), and Stargardt disease (SD).
View Article and Find Full Text PDFIEEE Trans Mol Biol Multiscale Commun
March 2025
Department of Pathology and Anatomical Sciences and Department of Biomedical Engineering, University at Buffalo, Buffalo, NY 14203 USA.
Cardiovascular diseases (CVDs) and pathologies are often driven by changes in molecular signaling and communication, as well as in cellular and tissue components, particularly those involving the extracellular matrix (ECM), cytoskeleton, and immune response. The fine-wire vascular injury model is commonly used to study neointimal hyperplasia and vessel stiffening, but it is not typically considered a model for CVDs. However, applying this model to study CVDs in conjunction with established processes could offer valuable insights.
View Article and Find Full Text PDFBMC Genomics
August 2025
School of Life Sciences/Hebei Basic Science Center for Biotic Interaction, Institute of Life Science and Green Development, Hebei University, Baoding, 071002, China.
Background: The kynurenine pathway (KP), central to tryptophan metabolism, regulates neuroimmune interactions in vertebrates through the dual actions of indoleamine 2,3-dioxygenase (IDO) and tryptophan 2,3-dioxygenase (TDO). However, crustaceans lack IDO and rely solely on TDO, yet the tissue-specific roles of TDO in this lineage remain unknown. Using Litopenaeus vannamei, a key aquaculture species, we investigated how TDO-mediated KP adapts to functional constraints in neural and respiratory tissues.
View Article and Find Full Text PDFCells
August 2025
Institut Recerca Sant Pau (IR-Sant Pau), 08041 Barcelona, Spain.
Mechanical and contractile forces in the vascular wall regulate smooth muscle cell migration. We previously demonstrated the presence of C3 complement products in atherosclerotic lesions of human aortas and showed that that C3-derived fragments promote key cellular processes, such as actin cytoskeleton organization and cell migration, in lipid-loaded human vascular smooth muscle cells (hVSMCs). In the present study, we aimed to investigate gene expression profiles related to cytoskeletal remodeling and cell adhesion in migrating hVSMCs with a particular focus on modulatory effect of the C3 complement pathway on these processes.
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