Relevant bibliographies by topics / Cell adhesion and migration

Academic literature on the topic 'Cell adhesion and migration'

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Published: 10 March 2023
Last updated: 11 March 2023

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Journal articles on the topic "Cell adhesion and migration"

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Aguilar-Cuenca, Rocio, Clara Llorente-Gonzalez, Carlos Vicente, and Miguel Vicente-Manzanares. "Microfilament-coordinated adhesion dynamics drives single cell migration and shapes whole tissues." F1000Research 6 (February 17, 2017): 160. http://dx.doi.org/10.12688/f1000research.10356.1.

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Cell adhesion to the substratum and/or other cells is a crucial step of cell migration. While essential in the case of solitary migrating cells (for example, immune cells), it becomes particularly important in collective cell migration, in which cells maintain contact with their neighbors while moving directionally. Adhesive coordination is paramount in physiological contexts (for example, during organogenesis) but also in pathology (for example, tumor metastasis). In this review, we address the need for a coordinated regulation of cell-cell and cell-matrix adhesions during collective cell migration. We emphasize the role of the actin cytoskeleton as an intracellular integrator of cadherin- and integrin-based adhesions and the emerging role of mechanics in the maintenance, reinforcement, and turnover of adhesive contacts. Recent advances in understanding the mechanical regulation of several components of cadherin and integrin adhesions allow us to revisit the adhesive clutch hypothesis that controls the degree of adhesive engagement during protrusion. Finally, we provide a brief overview of the major impact of these discoveries when using more physiological three-dimensional models of single and collective cell migration.
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Ventre, Maurizio, Carlo Fortunato Natale, Carmela Rianna, and Paolo Antonio Netti. "Topographic cell instructive patterns to control cell adhesion, polarization and migration." Journal of The Royal Society Interface 11, no. 100 (November 6, 2014): 20140687. http://dx.doi.org/10.1098/rsif.2014.0687.

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Topographic patterns are known to affect cellular processes such as adhesion, migration and differentiation. However, the optimal way to deliver topographic signals to provide cells with precise instructions has not been defined yet. In this work, we hypothesize that topographic patterns may be able to control the sensing and adhesion machinery of cells when their interval features are tuned on the characteristic lengths of filopodial probing and focal adhesions (FAs). Features separated by distance beyond the length of filopodia cannot be readily perceived; therefore, the formation of new adhesions is discouraged. If, however, topographic features are separated by a distance within the reach of filopodia extension, cells can establish contact between adjacent topographic islands. In the latter case, cell adhesion and polarization rely upon the growth of FAs occurring on a specific length scale that depends on the chemical properties of the surface. Topographic patterns and chemical properties may interfere with the growth of FAs, thus making adhesions unstable. To test this hypothesis, we fabricated different micropatterned surfaces displaying feature dimensions and adhesive properties able to interfere with the filopodial sensing and the adhesion maturation, selectively. Our data demonstrate that it is possible to exert a potent control on cell adhesion, elongation and migration by tuning topographic features’ dimensions and surface chemistry.
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Powner, Dale, Petra M. Kopp, Susan J. Monkley, David R. Critchley, and Fedor Berditchevski. "Tetraspanin CD9 in cell migration." Biochemical Society Transactions 39, no. 2 (March 22, 2011): 563–67. http://dx.doi.org/10.1042/bst0390563.

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Tetraspanin CD9 is associated with integrin adhesion receptors and it was reported that CD9 regulates integrin-dependent cell migration and invasion. Pro- and anti-migratory effects of CD9 have been linked to adhesion-dependent signalling pathways, including phosphorylation of FAK (focal adhesion kinase) and activation of phosphoinositide 3-kinase, p38 MAPK (mitogen-activated protein kinase) and JNK (c-Jun N-terminal kinase). In the present paper, we describe a novel mechanism whereby CD9 specifically controls localization of talin1, one of the critical regulators of integrin activation, to focal adhesions: CD9-deficiency leads to impaired localization of talin1 to focal adhesions and correlates with increased motility of breast cancer cells.
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Peacock, Justin G., Ann L. Miller, William D. Bradley, Olga C. Rodriguez, Donna J. Webb, and Anthony J. Koleske. "The Abl-related Gene Tyrosine Kinase Acts through p190RhoGAP to Inhibit Actomyosin Contractility and Regulate Focal Adhesion Dynamics upon Adhesion to Fibronectin." Molecular Biology of the Cell 18, no. 10 (October 2007): 3860–72. http://dx.doi.org/10.1091/mbc.e07-01-0075.

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In migrating cells, actin polymerization promotes protrusion of the leading edge, whereas actomyosin contractility powers net cell body translocation. Although they promote F-actin–dependent protrusions of the cell periphery upon adhesion to fibronectin (FN), Abl family kinases inhibit cell migration on FN. We provide evidence here that the Abl-related gene (Arg/Abl2) kinase inhibits fibroblast migration by attenuating actomyosin contractility and regulating focal adhesion dynamics. arg−/− fibroblasts migrate at faster average speeds than wild-type (wt) cells, whereas Arg re-expression in these cells slows migration. Surprisingly, the faster migrating arg−/− fibroblasts have more prominent F-actin stress fibers and focal adhesions and exhibit increased actomyosin contractility relative to wt cells. Interestingly, Arg requires distinct functional domains to inhibit focal adhesions and actomyosin contractility. The kinase domain–containing Arg N-terminal half can act through the RhoA inhibitor p190RhoGAP to attenuate stress fiber formation and cell contractility. However, Arg requires both its kinase activity and its cytoskeleton-binding C-terminal half to fully inhibit focal adhesions. Although focal adhesions do not turn over efficiently in the trailing edge of arg−/− cells, the increased contractility of arg−/− cells tears the adhesions from the substrate, allowing for the faster migration observed in these cells. Together, our data strongly suggest that Arg inhibits cell migration by restricting actomyosin contractility and regulating its coupling to the substrate through focal adhesions.
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Huttenlocher, A. "Adhesion in cell migration." Current Opinion in Cell Biology 7, no. 5 (1995): 697–706. http://dx.doi.org/10.1016/0955-0674(95)80112-x.

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Yamana, Norikazu, Yoshiki Arakawa, Tomohiro Nishino, Kazuo Kurokawa, Masahiro Tanji, Reina E. Itoh, James Monypenny, et al. "The Rho-mDia1 Pathway Regulates Cell Polarity and Focal Adhesion Turnover in Migrating Cells through Mobilizing Apc and c-Src." Molecular and Cellular Biology 26, no. 18 (September 15, 2006): 6844–58. http://dx.doi.org/10.1128/mcb.00283-06.

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ABSTRACT Directed cell migration requires cell polarization and adhesion turnover, in which the actin cytoskeleton and microtubules work critically. The Rho GTPases induce specific types of actin cytoskeleton and regulate microtubule dynamics. In migrating cells, Cdc42 regulates cell polarity and Rac works in membrane protrusion. However, the role of Rho in migration is little known. Rho acts on two major effectors, ROCK and mDia1, among which mDia1 produces straight actin filaments and aligns microtubules. Here we depleted mDia1 by RNA interference and found that mDia1 depletion impaired directed migration of rat C6 glioma cells by inhibiting both cell polarization and adhesion turnover. Apc and active Cdc42, which work together for cell polarization, localized in the front of migrating cells, while active c-Src, which regulates adhesion turnover, localized in focal adhesions. mDia1 depletion impaired localization of these molecules at their respective sites. Conversely, expression of active mDia1 facilitated microtubule-dependent accumulation of Apc and active Cdc42 in the polar ends of the cells and actin-dependent recruitment of c-Src in adhesions. Thus, the Rho-mDia1 pathway regulates polarization and adhesion turnover by aligning microtubules and actin filaments and delivering Apc/Cdc42 and c-Src to their respective sites of action.
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Longley, R. L., A. Woods, A. Fleetwood, G. J. Cowling, J. T. Gallagher, and J. R. Couchman. "Control of morphology, cytoskeleton and migration by syndecan-4." Journal of Cell Science 112, no. 20 (October 15, 1999): 3421–31. http://dx.doi.org/10.1242/jcs.112.20.3421.

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Syndecan-4 is a widely expressed transmembrane heparan sulfate proteoglycan which localizes to focal adhesions. Previous studies showed that the syndecan-4 cytoplasmic domain can associate with and potentiate the activity of protein kinase C, which is required for focal adhesion formation. To examine further the role of syndecan-4 in cell adhesion, we expressed syndecan-4 cDNA constructs in CHO-K1 cells. Syndecan-2 transfection was used to confirm effects seen were specific for syndecan-4. Cells overexpressing full length syndecan-4 core protein exhibited a more flattened, fibroblastic morphology, with increased focal adhesion formation and decreased cell motility. Expression of a syndecan-4 core protein with either a partial or complete deletion of the cytoplasmic domain or of an antisense construct led to markedly decreased spreading and focal adhesion formation, a more epithelioid morphology, and decreased motility. Overexpression of syndecan-2 changed the adhesive phenotype, but did not markedly alter focal adhesion and microfilament bundle formation. The data suggest that syndecan-4 is a regulator of focal adhesion and stress fiber formation, and influences both morphology and migration.
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González-Tarragó, Víctor, Alberto Elosegui-Artola, Elsa Bazellières, Roger Oria, Carlos Pérez-González, and Pere Roca-Cusachs. "Binding of ZO-1 to α5β1 integrins regulates the mechanical properties of α5β1–fibronectin links." Molecular Biology of the Cell 28, no. 14 (July 7, 2017): 1847–52. http://dx.doi.org/10.1091/mbc.e17-01-0006.

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Fundamental processes in cell adhesion, motility, and rigidity adaptation are regulated by integrin-mediated adhesion to the extracellular matrix (ECM). The link between the ECM component fibronectin (fn) and integrin α5β1 forms a complex with ZO-1 in cells at the edge of migrating monolayers, regulating cell migration. However, how this complex affects the α5β1-fn link is unknown. Here we show that the α5β1/ZO-1 complex decreases the resistance to force of α5β1–fn adhesions located at the edge of migrating cell monolayers while also increasing α5β1 recruitment. Consistently with a molecular clutch model of adhesion, this effect of ZO-1 leads to a decrease in the density and intensity of adhesions in cells at the edge of migrating monolayers. Taken together, our results unveil a new mode of integrin regulation through modification of the mechanical properties of integrin–ECM links, which may be harnessed by cells to control adhesion and migration.
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Wang, Chenlu, Sagar Chowdhury, Meghan Driscoll, Carole A. Parent, S. K. Gupta, and Wolfgang Losert. "The interplay of cell–cell and cell–substrate adhesion in collective cell migration." Journal of The Royal Society Interface 11, no. 100 (November 6, 2014): 20140684. http://dx.doi.org/10.1098/rsif.2014.0684.

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Collective cell migration often involves notable cell–cell and cell–substrate adhesions and highly coordinated motion of touching cells. We focus on the interplay between cell–substrate adhesion and cell–cell adhesion. We show that the loss of cell-surface contact does not significantly alter the dynamic pattern of protrusions and retractions of fast migrating amoeboid cells ( Dictyostelium discoideum ), but significantly changes their ability to adhere to other cells. Analysis of the dynamics of cell shapes reveals that cells that are adherent to a surface may coordinate their motion with neighbouring cells through protrusion waves that travel across cell–cell contacts. However, while shape waves exist if cells are detached from surfaces, they do not couple cell to cell. In addition, our investigation of actin polymerization indicates that loss of cell-surface adhesion changes actin polymerization at cell–cell contacts. To further investigate cell–cell/cell–substrate interactions, we used optical micromanipulation to form cell–substrate contact at controlled locations. We find that both cell-shape dynamics and cytoskeletal activity respond rapidly to the formation of cell–substrate contact.
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Sander, Eva E., Sanne van Delft, Jean P. ten Klooster, Tim Reid, Rob A. van der Kammen, Frits Michiels, and John G. Collard. "Matrix-dependent Tiam1/Rac Signaling in Epithelial Cells Promotes Either Cell–Cell Adhesion or Cell Migration and Is Regulated by Phosphatidylinositol 3-Kinase." Journal of Cell Biology 143, no. 5 (November 30, 1998): 1385–98. http://dx.doi.org/10.1083/jcb.143.5.1385.

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We previously demonstrated that both Tiam1, an activator of Rac, and constitutively active V12Rac promote E-cadherin–mediated cell–cell adhesion in epithelial Madin Darby canine kidney (MDCK) cells. Moreover, Tiam1 and V12Rac inhibit invasion of Ras-transformed, fibroblastoid MDCK-f3 cells by restoring E-cadherin–mediated cell–cell adhesion. Here we show that the Tiam1/Rac-induced cellular response is dependent on the cell substrate. On fibronectin and laminin 1, Tiam1/Rac signaling inhibits migration of MDCK-f3 cells by restoring E-cadherin–mediated cell– cell adhesion. On different collagens, however, expression of Tiam1 and V12Rac promotes motile behavior, under conditions that prevent formation of E-cadherin adhesions. In nonmotile cells, Tiam1 is present in adherens junctions, whereas Tiam1 localizes to lamellae of migrating cells. The level of Rac activation by Tiam1, as determined by binding to a glutathione-S-transferase– PAK protein, is similar on fibronectin or collagen I, suggesting that rather the localization of the Tiam1/Rac signaling complex determines the substrate-dependent cellular responses. Rac activation by Tiam1 requires PI3-kinase activity. Moreover, Tiam1- but not V12Rac-induced migration as well as E-cadherin–mediated cell– cell adhesion are dependent on PI3-kinase, indicating that PI3-kinase acts upstream of Tiam1 and Rac.
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Dissertations / Theses on the topic "Cell adhesion and migration"

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Burthem, John. "Hairy cell adhesion and migration." Thesis, University of Liverpool, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240394.

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Chen, Ning. "Role of cell adhesion molecules in melanoma transendothelial migration." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ58734.pdf.

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Baghdadchi, Negin. "CYTOKINE CONTROL OF GLIOMA ADHESION AND MIGRATION." CSUSB ScholarWorks, 2014. https://scholarworks.lib.csusb.edu/etd/93.

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Glioblastoma multiforme (GBM) is the most lethal primary central nervous system tumor, with median survival after diagnosis of less than 12 months because dissemination into the brain parenchyma limits the long-term effectiveness of surgical resection, and because GBM cells are resistant to radiation and chemotherapy. This sad dismal prognosis for patients with GBM emphasizes the need for greater understand of the fundamental biology of the disease. Invasion is one of the major causes of treatment failure and death from glioma, because disseminated tumor cells provide the seeds for tumor recurrence. Inflammation is increasingly recognized as an important component of invasion. In the brain, inflammation can occur by activation of microglia, the resident macrophages of the brain, or by tumor-associated blood macrophages. Therefore, we hypothesize that activity of the innate immune system in the brain can influence tumor progression by secreting cytokines such as Tumor Necrosis Factor alpha (TNF-α). In this study, we show that patient-derived glioma spheres undergo morphological changes in response to TNF‑α that are associated with changes in migration behavior in vitro. These morphological changes include appearance of tumor islands in site different from where the primary tumor cells were seeded. We further showed that TNF‑α treated cells significantly increased expression of cell adhesion molecules such as CD44 and VCAM-1. Furthermore, we demonstrate increased cell density also caused increased in expression of cell adhesion molecules. The extent to which these are recapitulated in vivo will be investigated.
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Chon, John H. "Mediation of vascular smooth muscle cell adhesion and migration by cell surface heparan sulfate glycosaminoglycans." Diss., Georgia Institute of Technology, 1999. http://hdl.handle.net/1853/11315.

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Li, ShuShun. "Thrombospondin 1, an autocrine regulator in T cell adhesion and migration." Doctoral thesis, Umeå : Klinisk mikrobiologi, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-599.

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Vielkind, Susina. "Role of the GTPase Rho in T cell adhesion and migration." Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406052.

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Rabut, Anne. "Regulation of Drosophila E-cadherin mediated adhesion during border cell migration." Université Louis Pasteur (Strasbourg) (1971-2008), 2004. https://publication-theses.unistra.fr/public/theses_doctorat/2004/RABUT_Anne_2004.pdf.

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Au cours du développement, les cadhérines sont des médiateurs importants de l'adhérence entre cellules. Dans de nombreux processus développementaux, ces interactions intercellulaires sont très probablement régulées. De multiples mécanismes régulateurs de l'adhérence intercellulaire ont été étudiés dans des cellules en culture ; leur signification physiologique n'est cependant pas connue. Nous avons utilisé la Drosophile comme modèle d'étude de ces mécanismes in vivo. Nous avons généré plusieurs formes mutantes de la DE-cadhérine (Drosophila Epithelial Cadherin) et testé leur capacité à remplacer la DE-cadhérine endogène au cours du développement et de l'ovogenèse, en particulier au cours de la migration des cellules de bordure. Différents mutants DE-cadhérine nous ont permis de montrer que ni l'interaction entre la DE-cadhérine et p120ctn, ni le domaine juxtamembranaire de la DE-cadhérine, ni les tyrosines conservées présentes dans le domaine cytoplasmique ne sont essentielles pour la fonction de la DE-cadhérine. DE-cadhérine-Db/a-caténine (a-caténine fusionnée après le domaine juxtamembranaire de la DE-cadhérine) se substitue partiellement à la DE-cadhérine endogène dans les cellules de bordure, montrant que la régulation du lien entre la DE-cadhérine et a-caténine n'est pas strictement nécessaire à la migration. DE-cadhérine-DCyt/a-caténine (a-caténine fusionnée après le domaine transmembranaire de la DE-cadhérine) se substitue à la DE-cadhérine endogène dans l'épithélium folliculaire mais pas dans les cellules de bordure, suggérant que des signaux régulateurs importants pour la migration pourraient être présents dans le domaine cytoplasmique. Des expériences supplémentaires seront nécessaires pour confirmer que les défauts de migration observés avec DE-cadhérine-DCyt/a-caténine sont bien dus à une absence de régulation. Si cela s'avère être le cas, il restera à identifier plus précisement le(s) mécanisme(s) régulant DE-cadhérine dans les cellules de bordure
Classic cadherins are major mediators of homophilic cell-cell adhesion during animal development. In many developmental processes cadherin-dependent adhesive interactions between cells are likely to be regulated. A lot has been done to understand how adhesion is regulated in tissue culture experiments, but so far little is known about the relevance of the studied regulatory mechanisms in vivo. We used Drosophila as a model to study these putative regulatory mechanisms during development. Several mutant variants of Drosophila Epithelial cadherin (DE-cadherin) were generated. Their ability to substitute for endogenous DE-cadherin activity was analyzed in multiple cadherin-dependent processes during Drosophila development and oogenesis, in particular during border cell migration, a process that probably requires dynamic adhesion. Using different DE-cadherin variants, I showed that DE-cadherin/p120ctn interaction, DE-cadherin juxtamembrane domain as well as the conserved tyrosines in DE-cadherin cytoplasmic domain are surprisingly all dispensable for DE-cadherin function. DE-cadherin-Db/a-catenin (a-catenin fused after DE-cadherin juxtamembrane domain) partially substitutes for endogenous DE-cadherin in border cells, showing that regulation of the link between DE-cadherin and a-catenin is not strictly required for the migration. DE-cadherin-DCyt/a-catenin (a-catenin fused after DE-cadherin transmembrane domain) is able to mediate adhesion in the follicular epithelium but does not substitute for endogenous DE-cadherin in border cells, suggesting that some regulatory signals important for the migration may be located in DE-cadherin cytoplasmic domain. However, DE-cadherin-DCyt/a-catenin also have some clear subcellular localization defects and it is so far not completely clear if the observed migration defects are really due to lack of adhesion regulation. If this is the case, the precise regulatory mechanisms will still need to be identified
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Lee, Eun-ju Yousaf Muhammad. "Development of dynamic substrates for studies of cell adhesion and migration." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2009. http://dc.lib.unc.edu/u?/etd,2284.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2009.
Title from electronic title page (viewed Jun. 26, 2009). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Chemistry." Discipline: Chemistry; Department/School: Chemistry.
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Bliss, Katherine Theresa. "Elucidating the Role of Lasp-2 in Cell Adhesion and Migration." Diss., The University of Arizona, 2012. http://hdl.handle.net/10150/255198.

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In order for cells to migrate, communicate, and facilitate attachment to the surrounding extraceullar matrix, they must form intricate protein complexes called focal adhesions. The number of identified focal adhesion components continues to grow and the field is an area of active study.Lasp-2 is a member of the nebulin family of actin-binding proteins that has been identified as a member of focal adhesion complexes. To gain further insights into the functional role of lasp-2, we identified two additional binding partners of lasp-2, the integral focal adhesion proteins, vinculin and paxillin. Interestingly, the interaction of lasp-2 with its binding partners vinculin and paxillin was significantly reduced in presence of lasp-1, another nebulin family member. The presence of lasp-2 appears to enhance the interaction of vinculin and paxillin with each other, however, as with the interaction of lasp-2 with vinculin or paxillin, this effect is greatly diminished in the presence of excess lasp-1 suggesting the interplay between lasp-2 and lasp-2 could be an adhesion regulatory mechanism. Lasp-2's potential role in metastasis was revealed as overexpression of lasp-2 in SW620 cells, a highly metastatic cancer cell line, increased cell migration, but impeded cell invasion.Lasp-2 transcript and protein is readily detected in neural tissues. Preliminary experiments involving the knockdown of lasp-2- in frog embryos revealed gross morphological abnormalities in the head region as well as the inability to move normally. Neural crest derived melanocytes also failed to migrate normally.Taken together, these data suggest that lasp-2 has an important role in coordinating and regulating the composition and dynamics of focal adhesions.
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FERRARIS, G. M. SARRA. "NON-INTEGRIN CELL ADHESION TRIGGERS LIGAND-INDEPENDENT INTEGRIN SIGNALING." Doctoral thesis, Università degli Studi di Milano, 2011. http://hdl.handle.net/2434/157459.

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Integrins are the major family of cell surface adhesion receptors responsible for the regulation of the physical contact and biochemical communication between the cell and the surrounding extracellular matrix (ECM). Binding of the extracellular domains of integrins to components in the ECM triggers a series of molecular events commonly referred to as “outside-in” signaling, leading to context-dependent changes in cell morphology, migration and proliferation. In this prevailing paradigm of cell adhesion induced signaling the primary functions of the integrin is to provide the physical transmembrane bridge connecting the intracellular signaling machinery and cytoskeleton to the extracellular environment. We now present evidence that most, if not all, cell adhesion receptors trigger integrin-dependent outside-in signaling independently of direct contacts between the integrins and their ligands in the ECM. The urokinase-type plasminogen activator receptor (uPAR/CD87) is a non-integrin vitronectin (VN) cell adhesion receptor linked to the outer membrane leaflet by a GPI-anchor. Through an extensive structure-function analysis of uPAR, VN, β1 and β3 we document that cell adhesion induced by the uPAR/VN-interaction triggers integrin-mediated, but ligand independent, cell spreading and signaling. This signaling is fully active on VN lacking functional integrin binding sites and by integrin mutants deficient in ligand binding, but is crucially dependent on an “active” conformation of the integrin as well as its binding to intracellular adaptor proteins including talin and kindlin. This novel paradigm of ligand-independent integrin signaling is not restricted to uPAR as it poses no identifiable constraints to the adhesion receptor with respect to ternary-structure, ligand type or means of membrane anchorage. In full accordance with a general validity of this paradigm, we show that cell adhesion physically mediated by a signaling-incompetent β3 integrin is effectively translated into cell spreading and signaling by the β1 integrin. Our results show that integrins are active in transducing adhesion-induced signaling in the absence of their cognate ligands, suggesting that the bi-directional signaling capability of these receptors may have evolved primarily to allow for tightly regulated inside-out signaling.
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Books on the topic "Cell adhesion and migration"

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McGrath, John. CELL ADHESION AND MIGRATION IN SKIN DISEASE. Edited by Jonathan Barker. Abingdon, UK: Taylor & Francis, 2001. http://dx.doi.org/10.4324/9780203304594.

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Chen, Ning. Role of cell adhesion molecules in melanoma transendothelial migration. Ottawa: National Library of Canada, 2001.

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Hennigan, Shauna M. The effects of transendothelial migration on neutrophil function and programmed cell death. Dublin: University College Dublin, 1996.

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Behrens, Jürgen, and W. James Nelson, eds. Cell Adhesion. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-540-68170-0.

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C, Beckerle Mary, ed. Cell adhesion. New York: Oxford University Press, 2001.

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Bongrand, Pierre, Per M. Claesson, and Adam S. G. Curtis, eds. Studying Cell Adhesion. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-662-03008-0.

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Berezin, Vladimir, and Peter S. Walmod, eds. Cell Adhesion Molecules. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8090-7.

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Hemler, Martin E., and Enrico Mihich, eds. Cell Adhesion Molecules. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2830-2.

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Pierre, Bongrand, Claesson P. M, and Curtis A. S. G, eds. Studying cell adhesion. Berlin: Springer-Verlag, 1994.

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G, Curtis A. S., Lackie J. M, and Council of Europe, eds. Measuring cell adhesion. Chichester, West Sussex, England: Wiley, 1991.

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Book chapters on the topic "Cell adhesion and migration"

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Mondal, Chandrani, Julie Di Martino, and Jose Javier Bravo-Cordero. "Imaging Cell Adhesion and Migration." In Imaging from Cells to Animals In Vivo, 211–20. First edition. | Boca Raton : CRC Press, 2020. | Series: Series in cellular and clinical imaging: CRC Press, 2020. http://dx.doi.org/10.1201/9781315174662-15.

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Carman, Christopher V. "High-Resolution Fluorescence Microscopy to Study Transendothelial Migration." In Integrin and Cell Adhesion Molecules, 215–45. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-166-6_15.

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Rovensky, Yury A. "Cell Migration." In Adhesive Interactions in Normal and Transformed Cells, 121–44. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-304-2_6.

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Guadagno, Noemi A., and Cinzia Progida. "Probing the ER-Focal Adhesion Link During Cell Migration." In Cell Migration in Three Dimensions, 39–50. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2887-4_3.

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Lacoste, J., K. Young, and Claire M. Brown. "Live-Cell Migration and Adhesion Turnover Assays." In Methods in Molecular Biology, 61–84. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-056-4_3.

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Bosanquet, David C., Keith G. Harding, and Wen G. Jiang. "ECIS, Cellular Adhesion and Migration in Keratinocytes." In Electric Cell-Substrate Impedance Sensing and Cancer Metastasis, 217–37. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4927-6_12.

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Strutt, David, Ralf Schnabel, Franziska Fiedler, and Simone Prömel. "Adhesion GPCRs Govern Polarity of Epithelia and Cell Migration." In Adhesion G Protein-coupled Receptors, 249–74. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-41523-9_11.

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Shulman, Ziv, and Ronen Alon. "Real-Time Analysis of Integrin-Dependent Transendothelial Migration and Integrin-Independent Interstitial Motility of Leukocytes." In Integrin and Cell Adhesion Molecules, 31–45. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-166-6_3.

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Gunzer, M. "Migration, Cell–Cell Interaction and Adhesion in the Immune System." In Sparking Signals, 97–137. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/2789_2007_062.

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Menke, Andre, and Klaudia Giehl. "Regulation of the E-Cadherin Adhesion Complex in Tumor Cell Migration and Invasion." In Cell Migration: Signalling and Mechanisms, 120–35. Basel: KARGER, 2009. http://dx.doi.org/10.1159/000274480.

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Conference papers on the topic "Cell adhesion and migration"

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Han, Sangyoon J., and Nathan J. Sniadecki. "Traction Forces During Cell Migration Predicted by the Multiphysics Model." In ASME 2011 International Mechanical Engineering Congress and Exposition. ASMEDC, 2011. http://dx.doi.org/10.1115/imece2011-63843.

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Cells rely on traction forces in order to crawl across a substrate. These traction forces come from dynamic changes in focal adhesions, cytoskeletal structures, and chemical and mechanical signals from the extracellular matrix. Several computational models have been developed that help explain the trajectory or accumulation of cells during migration, but little attention has been placed on traction forces during this process. Here, we investigated the spatial and temporal dynamics of traction forces by using a multiphysics model that describes the cycle of steps for a migrating cell on an array of posts. The migration cycle includes extension of the leading edge, formation of new adhesions at the front, contraction of the cytoskeleton, and the release of adhesions at the rear. In the model, an activation signal triggers the assembly of actin and myosin into a stress fiber, which generates a cytoskeletal tension in a manner similar to Hill’s muscle model. In addition, the role that adhesion dynamics has in regulating cytoskeletal tension has been added to the model. The multiphysics model was simulated in Matlab for 1-D simulations, and in Comsol for 2-D simulations. The model was able to predict the spatial distribution of traction forces observed with previous experiments in which large forces were seen at the leading and trailing edges. The large traction force at the trailing edge during the extension phase likely contributes to detachment of the focal adhesion by overcoming its adhesion strength with the post. Moreover, the model found that the mechanical work of a migrating cell underwent a cyclic relationship that rose with the formation of a new adhesion and fell with the release of an adhesion at its rear. We applied a third activation signal at the time of release and found it helped to maintain a more consistent level of work during migration. Therefore, the results from both our 1-D and 2-D migration simulations strongly suggest that cells use biochemical activation to supplement the loss in cytoskeletal tension upon adhesion release.
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Zielinski, Rachel, Cosmin Mihai, and Samir Ghadiali. "Multi-Scale Modeling of Cancer Cell Migration and Adhesion During Epithelial-to-Mesenchymal Transition." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53511.

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Cancer is a leading cause of death in the US, and tumor cell metastasis and secondary tumor formation are key factors in the malignancy and prognosis of the disease. The regulation of cell motility plays an important role in the migration and invasion of cancer cells into surrounding tissues. The primary modes of increased motility in cancerous tissues may include collective migration of a group of epithelial cells during tumor growth and single cell migration of mesenchymal cells after detachment from the primary tumor site [1]. In epithelial cancers, metastasizing cells lose their cell-cell adhesions, detach from the tumor mass, begin expressing mesenchymal markers, and become highly motile and invasive, a process known as epithelial-to-mesenchymal transition (EMT) (Fig. 1) [2]. Although the cellular and biochemical signaling mechanisms underlying EMT have been studied extensively, there is limited information about the biomechanical mechanisms of EMT. In particular, it is not known how changes in cell mechanics (cell stiffness, cell-cell adhesion strength, traction forces) influence the detachment, migration and invasion processes that occur during metastasis.
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Baker, Brendon M., Colin K. Choi, Britta Trappmann, and Christopher S. Chen. "Engineered Fibrillar Extracellular Matrices for the Study of Directed Cell Migration." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80943.

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The biology of cell adhesion and migration has traditionally been studied on 2D glass or plastic surfaces. While such studies have shed light on the molecular mechanisms governing these processes [1], current knowledge is limited by the dissimilarity between the flat surfaces conventionally employed and the topographically complex extracellular matrix (ECM) cells routinely navigate within the body. On ECM-coated flat surfaces, cells are presented with an unlimited expanse of adhesive ligand and can spread and migrate freely. Conversely, the availability of ligand in vivo is generally restricted to ECM structures, forcing cells to form adhesions in prescribed locations distributed through 3D space depending on the geometry and organization of the surrounding matrix [2]. These physical constraints on cell adhesion likely have profound consequences on intracellular signaling and resulting migration, and calls into question whether the mechanisms and modes of cell motility observed on flat substrates are truly reflective of the in vivo scenario [3]. The topographies of ECMs found in vivo are varied but largely fibrillar, ranging from the tightly crosslinked fibers that form the sheet-like basement membrane, to the structure of fibrin-rich clots and collagenous connective tissues. Collagen comprises approximately 25% of the human body by mass, and as such, purified collagen has served as a popular setting for the study of cell migration within a fibrillar context for many decades [4]. However, a major limitation to the use of these gels is the inability to orthogonally dictate key structural features that impact cell behavior. For example, in contrast to the large range of fiber diameters found in vivo within connective tissue resulting from hierarchical collagen assembly and multiple types of collagens [3], collagen gels are limited to fibril diameters of ∼500nm. Furthermore, recreating the structural anisotropy common to connective tissues in collagen gels is technically challenging [5]. Thus, there remains a significant need for engineered fibrillar materials that afford precise and independent control of architectural and mechanical features for application in cell biology. In this work, we develop two approaches to fabricating fibrillar ECMs in order to study cell adhesion and migration in vitro.
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Hu, Jia, and Yaling Liu. "Cell Adhesion on a Wavy Surface." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14059.

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The ability to control the position of cells in an organized pattern on a substrate has become increasingly important for biosensing and tissue engineering applications [1–3]. With the advent of nanofabrication techniques, a number of researchers have studied the effects of nano-scale grooves on cell spreading, migration, morphology, signaling and orientation [4–6]. Recent studies have shown that cell adhesion/spreading can be influenced by a nanostructured surface [7]. In most current studies, the pattern dimensions are much smaller than the size of a cell. In this paper, we focus on studying cell response to micro scale patterns instead of nano-scale patterns.
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Shiraishi, Toshihiko, and Tomohiro Fukuno. "Cell Response to Cyclic Strain at Focal Adhesions." In ASME 2016 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/imece2016-66843.

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Cells are known to sense and respond to mechanical stimulations. The fact shows that there are some cellular mechanosensors for mechanical stimulations. One of the candidates of the mechanosensors is focal adhesions which are large macromolecular assemblies via which mechanical force and regulatory signals may be transmitted between the extracellular matrix and an interacting cell. Although it is quite important to clarify the mechanism of sensing and responding to the mechanical vibration via focal adhesions, there was no micro device applying time-varied mechanical loading to a single focal adhesion of the order of a micrometer. In order to solve the challenging issue, we developed a magnetic micropillar substrate which is able to apply cyclic strain to focal adhesions of a cell. Using the substrate, we investigated how a single osteoblast-like cell changed the direction of migration on micropillars cyclically deflected at 5 Hz and revealed the relationship between the cell migration and the traction force. The experimental results indicate that a cell may sense the cyclic strain and reduce the traction force which is not enough to move the cell body forward leading to changing the migration direction toward the place without cyclic strain.
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Jin, Quan, Claude Verdier, Pushpendra Singh, Nadine Aubry, and Alain Duperray. "Direct Simulation of the Migration of Leukocytes in Pressure Driven Flow." In ASME 2006 2nd Joint U.S.-European Fluids Engineering Summer Meeting Collocated With the 14th International Conference on Nuclear Engineering. ASMEDC, 2006. http://dx.doi.org/10.1115/fedsm2006-98415.

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We use the direct numerical simulation (DNS) approach to study the motion and deformation of leukocytes in pressure driven flows in a parallel plate channel in the case where there is an adhesion force between the leukocytes and the channel wall and when the adhesion force is absent. Two composite fluid models, consisting of a membrane, cytoplasm and a nucleus, are used to describe leukocytes. The first is the composite-drop model in which the cytoplasm and the nucleus are modeled as fluids, and the second is the drop-rigid-particle model in which the cytoplasm is modeled as a fluid and the nucleus as a rigid particle. The cytoplasm is modeled as a Newtonian fluid. The nucleus in the first model is assumed to be a viscoelastic liquid. The adhesion force is computed using two adhesion force models. In the first model, the adhesion force is given by a potential that varies as the fourth power of the distance between the cell and the adhesive wall. In the second model, the adhesion force is given by the Dembo’s kinetic adhesion model. The numerical code is based on the finite element method and the level-set method is used to track the cell membrane position. In the absence of the adhesion force, the equilibrium location of a freely suspended leukocyte in a pressure driven flow in a channel is shown to depend on the ratio of the cell to plasma viscosities. In presence of the adhesion force, the leukocyte is attracted to the layer of endothelial cells and, as it gets closer, it also deforms to get flatter under the shear forces. This deformation, in turn, further increases the adhesion force.
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Na, Sungsoo. "Engineering Tools for Studying Coordination Between Biochemical and Biomechanical Activities in Cell Migration." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53709.

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Cell migration is achieved by the dynamic feedback interactions between traction forces generated by the cell and exerted onto the underlying extracellular matrix (ECM), and intracellular mechano-chemical signaling pathways, e.g., Rho GTPase (RhoA, Rac1, and Cdc42) activities [1,2,3]. These components are differentially distributed within a cell, and thus the coordination between tractions and mechanotransduction (i.e, RhoA and Rac1 activities) must be implemented at a precise spatial and temporal order to achieve optimized, directed cell migration [4,5]. Recent studies have shown that focal adhesions at the leading edge exert strong tractions [6], and these traction sites are co-localized with focal adhesion sites [7]. Further, by using the fluorescence resonance energy transfer (FRET) technology coupled with genetically encoded biosensors, researchers reported that Rho GTPases, such as RhoA [8], Rac1 [9], and Cdc42 [10] are maximally activated at the leading edge, suggesting the leading edge of the cell as its common functional site for Rho GTPase activities. All these works, however, were done separately, and the relationship between tractions and mechanotransduction during cell migration has not been demonstrated directly because of the difficulty in simultaneously recording tractions and mechanotransduction in migrating cells, precluding direct comparison between these results. Furthermore, these studies have been conducted by monitoring cells on glass coverslips, the stiffness of which is ∼ 65 giga pascal (GPa), at least three to six order higher than the physiological range of ECM stiffness. Although it is increasingly accepted that ECM stiffness influences cell migration, it is not known exactly how physiologically relevant ECM stiffness (order of kPa range) affects the dynamics of RhoA and Rac1 activities. For a complete understanding of the mechanism of mechano-chemical signaling in the context of cell migration, the dynamics and interplay between biomechanical (e.g., tractions) and biochemical (e.g., Rho GTPase) activities should be visualized within the physiologically relevant range of ECM stiffness.
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To, Ciric, and Gianni M. Di Guglielmo. "Abstract 466: Synthetic triterpenoids target cell migration and cell adhesion via GSK3β." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-466.

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Pathak, Amit, and Sanjay Kumar. "A Multiscale Model of Cell Adhesion and Migration on Extracellular Matrices of Defined Stiffness and Adhesivity." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53757.

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Eukaryotic cells actively respond to variations in ligand density and stiffness of their extracellular matrix (ECM). This cell-ECM relationship plays an important role in regulating cell migration, wound healing, tumor invasion and metastasis. A better understanding of these mechanosenstive responses requires more rigorous models of the relationships between ECM biophysical properties, mechanotransductive signals, assembly of contractile and adhesive structures, and cell migration.
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Mai, Junyu, Song Li, and Xiang Zhang. "Protein Dot Array Patterning for Study of Cell Adhesion and Migration." In 2007 International Nano-Optoelectronics Workshop (iNOW). IEEE, 2007. http://dx.doi.org/10.1109/inow.2007.4302938.

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Reports on the topic "Cell adhesion and migration"

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Haugh, Jason M. Integration of Soluble and Adhesive Gradient Signals in Directed Cell Migration. Fort Belvoir, VA: Defense Technical Information Center, November 2006. http://dx.doi.org/10.21236/ada467054.

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Chen, Chen, Peng Chen, Xia Liu, and Hua Li. Combined 5-Fluorouracil and Low Molecular Weight Heparin for the Prevention of Postoperative Proliferative Vitreoretinopathy in Patients with Retinal Detachment. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0117.

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Review question / Objective: The aim of this meta-analysis is to evaluate the efficacy and safety of intraoperative infusion of combined 5-fluorouracil and low molecular weight heparin (LMWH) for the prevention of postoperative proliferative vitreoretinopathy in patients with retinal detachment. Condition being studied: Postoperative proliferative vitreoretinopathy (PVR) is the primary cause of failure of retinal reattachment surgery. 5-fluorouracil (5-FU) inhibits the proliferation of fibroblasts, and suppresses collagen contraction. On the other hand, heparin reduces fibrin exudation, and inhibits the adhesion and migration of retinal pigment epithelial cells. We conduct this comprehensive literature search and meta-analysis to address whether intraoperative infusion of combined 5-FU and LWMH improves the primary success rate of pars plana vitrectomy, as well as reduces postoperative PVR. Our study aims to provide clinical evidence for retinal surgeons concerning their choice of intraoperative medication.
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Byers, Stephen W. Cell-Cell Adhesion and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2000. http://dx.doi.org/10.21236/ada395237.

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Byers, Stephen W. Cell-Cell Adhesion and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 1999. http://dx.doi.org/10.21236/ada371168.

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Byers, Stephen W. Cell-Cell Adhesion and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 1998. http://dx.doi.org/10.21236/ada345188.

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Surmacz, Eva. IGF-IR, Cell Adhesion and Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada400067.

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Surmacz, Eva. IGF-IR, Cell Adhesion and Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada420246.

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Surmacz, Ewa. IGF-IR, Cell Adhesion and Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2000. http://dx.doi.org/10.21236/ada392765.

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Park, Electa R., Alexis L. Bergsma, and Amanda L. Erwin. CD82 and Cell-Cell Adhesion in Metastatic Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada588246.

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Bertozzi, Carolyn R. Metabolic Engineering of Reactive Cell Surfaces for Controlled Cell Adhesion. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada421093.

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