Relevant bibliographies by topics / Leader cells in cell migration

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Academic literature on the topic 'Leader cells in cell migration'

Author: Grafiati
Published: 6 September 2023

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Journal articles on the topic "Leader cells in cell migration"

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Qin, Lei, Dazhi Yang, Weihong Yi, Huiling Cao, and Guozhi Xiao. "Roles of leader and follower cells in collective cell migration." Molecular Biology of the Cell 32, no. 14 (July 1, 2021): 1267–72. http://dx.doi.org/10.1091/mbc.e20-10-0681.

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Collective cell migration is a widely observed phenomenon during animal development, tissue repair, and cancer metastasis. Considering its broad involvement in biological processes, it is essential to understand the basics behind the collective movement. Based on the topology of migrating populations, tissue-scale kinetics, called the “leader–follower” model, has been proposed for persistent directional collective movement. Extensive in vivo and in vitro studies reveal the characteristics of leader cells, as well as the special mechanisms leader cells employ for maintaining their positions in collective migration. However, follower cells have attracted increasing attention recently due to their important contributions to collective movement. In this Perspective, the current understanding of the molecular mechanisms behind the “leader–follower” model is reviewed with a special focus on the force transmission and diverse roles of leaders and followers during collective cell movement.
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Khalil, Antoine A., and Peter Friedl. "Determinants of leader cells in collective cell migration." Integrative Biology 2, no. 11-12 (2010): 568. http://dx.doi.org/10.1039/c0ib00052c.

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Xin, Zhuohan, Keiko Deguchi, Shin-ichiro Suye, and Satoshi Fujita. "Quantitative Analysis of Collective Migration by Single-Cell Tracking Aimed at Understanding Cancer Metastasis." International Journal of Molecular Sciences 23, no. 20 (October 15, 2022): 12372. http://dx.doi.org/10.3390/ijms232012372.

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Metastasis is a major complication of cancer treatments. Studies of the migratory behavior of cells are needed to investigate and control metastasis. Metastasis is based on the epithelial–mesenchymal transition, in which epithelial cells acquire mesenchymal properties and the ability to leave the population to invade other regions of the body. In collective migration, highly migratory “leader” cells are found at the front of the cell population, as well as cells that “follow” these leader cells. However, the interactions between these cells are not well understood. We examined the migration properties of leader–follower cells during collective migration at the single-cell level. Different mixed ratios of “leader” and “follower” cell populations were compared. Collective migration was quantitatively analyzed from two perspectives: cell migration within the colony and migration of the entire colony. Analysis of the effect of the cell mixing ratio on migration behavior showed that a small number of highly migratory cells enhanced some of the migratory properties of other cells. The results provide useful insights into the cellular interactions in collective cell migration of cancer cell invasion.
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Cao, Yanyang, Priscilla Y. Hwang, Maria Clarke, Jose Almeida, Amit Pathak, and Gregory D. Longmore. "Abstract 2423: A Cdh3 - Lam332 signaling axis by a unique subset of leader cells controls breast tumor organoid protrusion dynamics and directed collective migration." Cancer Research 82, no. 12_Supplement (June 15, 2022): 2423. http://dx.doi.org/10.1158/1538-7445.am2022-2423.

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Abstract Carcinoma dissemination can occur when heterogeneous tumor and tumor stromal cells clusters migrate together via collective migration. Cells at the front lead and direct collective migration, yet how these leader cells form and interact with the microenvironment to direct migration are not fully appreciated. From live videos of primary mouse and human breast tumor organoids in a 3D microfluidic system that mimics the native breast tumor microenvironment, we developed 3D computational models. These hypothesize that for leader cells to polarize to the leading edge and lead directed collective migration they need to generate high protrusive forces and overcome extracellular matrix (ECM) resistance. From scRNAseq of migrating primary tumor organoids, we identify significant K14+ “leader” cell heterogeneity that differs depending upon the environmental signal. We isolate a unique Cadherin-3 (Cdh3) positive leader cell subpopulation that is necessary and sufficient to lead collective migration. Cdh3 controls leader cell protrusion dynamics through controlling the local production of Laminin-332 which is required for integrin/focal adhesion function. Loss of Cdh3 expression in mouse and human primary breast tumor organoids and invasive breast tumor cell lines significantly impairs directed collective migration. In the absence of leader cell Cdh-Cdh3 intercellular adhesions there is reduced cellular β-catenin levels and Laminin 332 production. In syngeneic, orthotopic transplant mouse models, Cdh3 depletion in tumor cells resulted in decreased laminin 332 production at the invasive edge of primary tumors and decreased lung metastasis. Chromatin Immunoprecipitation experiments revealed that in contacted cells β-catenin and TCF4 are present on Lam α3, β3, and γ2 promoter regions. Laminin 332 production by leader cells was required for optimal Integrin/FA function and cellular protrusion stability. These results indicated that in leader cells local Cdh3-Cdh3/β-catenin regulated Laminin 332 production controls protrusion dynamics and overcomes resistance to ECM to lead directed collective tumor migration. Our findings highlight how a unique subset of leader cells in breast tumors interact with the microenvironment to direct collective migration. Citation Format: Yanyang Cao, Priscilla Y. Hwang, Maria Clarke, Jose Almeida, Amit Pathak, Gregory D. Longmore. A Cdh3 - Lam332 signaling axis by a unique subset of leader cells controls breast tumor organoid protrusion dynamics and directed collective migration [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2423.
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Theveneau, Eric, and Claudia Linker. "Leaders in collective migration: are front cells really endowed with a particular set of skills?" F1000Research 6 (October 27, 2017): 1899. http://dx.doi.org/10.12688/f1000research.11889.1.

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Collective cell migration is the coordinated movement emerging from the interaction of at least two cells. In multicellular organisms, collective cell migration is ubiquitous. During development, embryonic cells often travel in numbers, whereas in adults, epithelial cells close wounds collectively. There is often a division of labour and two categories of cells have been proposed: leaders and followers. These two terms imply that followers are subordinated to leaders whose proposed broad range of actions significantly biases the direction of the group of cells towards a specific target. These two terms are also tied to topology. Leaders are at the front while followers are located behind them. Here, we review recent work on some of the main experimental models for collective cell migration, concluding that leader-follower terminology may not be the most appropriate. It appears that not all collectively migrating groups are driven by cells located at the front. Moreover, the qualities that define leaders (pathfinding, traction forces and matrix remodelling) are not specific to front cells. These observations indicate that the terms leaders and followers are not suited to every case. We think that it would be more accurate to dissociate the function of a cell from its position in the group. The position of cells can be precisely defined with respect to the direction of movement by purely topological terms such as “front” or “rear” cells. In addition, we propose the more ample and strictly functional definition of “steering cells” which are able to determine the directionality of movement for the entire group. In this context, a leader cell represents only a specific case in which a steering cell is positioned at the front of the group.
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De Pascalis, Chiara, Carlos Pérez-González, Shailaja Seetharaman, Batiste Boëda, Benoit Vianay, Mithila Burute, Cécile Leduc, Nicolas Borghi, Xavier Trepat, and Sandrine Etienne-Manneville. "Intermediate filaments control collective migration by restricting traction forces and sustaining cell–cell contacts." Journal of Cell Biology 217, no. 9 (July 6, 2018): 3031–44. http://dx.doi.org/10.1083/jcb.201801162.

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Mesenchymal cell migration relies on the coordinated regulation of the actin and microtubule networks that participate in polarized cell protrusion, adhesion, and contraction. During collective migration, most of the traction forces are generated by the acto-myosin network linked to focal adhesions at the front of leader cells, which transmit these pulling forces to the followers. Here, using an in vitro wound healing assay to induce polarization and collective directed migration of primary astrocytes, we show that the intermediate filament (IF) network composed of vimentin, glial fibrillary acidic protein, and nestin contributes to directed collective movement by controlling the distribution of forces in the migrating cell monolayer. Together with the cytoskeletal linker plectin, these IFs control the organization and dynamics of the acto-myosin network, promoting the actin-driven treadmilling of adherens junctions, thereby facilitating the polarization of leader cells. Independently of their effect on adherens junctions, IFs influence the dynamics and localization of focal adhesions and limit their mechanical coupling to the acto-myosin network. We thus conclude that IFs promote collective directed migration in astrocytes by restricting the generation of traction forces to the front of leader cells, preventing aberrant tractions in the followers, and by contributing to the maintenance of lateral cell–cell interactions.
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Caruso, Alexa, Neelakshi Kar, and Jeremy Logue. "Abstract B021: Piezo1 and ROCK2 promote fast amoeboid migration in confined environments." Cancer Research 83, no. 2_Supplement_2 (January 15, 2023): B021. http://dx.doi.org/10.1158/1538-7445.metastasis22-b021.

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Abstract Cell migration through confined environments may induce a phenotypic transition to fast amoeboid (leader bleb-based) migration. However, the molecular mechanism(s) controlling this phenotypic transition remain poorly understood. Here, we show that regulation of intracellular calcium levels by the plasma membrane tension sensor, Piezo1, promotes the Leader Bleb-Based Migration (LBBM) of melanoma cells. Using a ratiometric assay, intracellular calcium is shown to rise with increasing levels of confinement. Chelation of extracellular and intracellular calcium by BAPTA and BAPTA-AM, respectively, inhibits LBBM. Moreover, in highly motile cells, we found intracellular calcium levels to be dramatically increased at the cell rear. Using the Piezo1 inhibitor, GsMTx4, and RNAi, we can inhibit the phenotypic transition to fast amoeboid (leader bleb-based) migration. Therefore, we wondered if Piezo1 through calcium/calmodulin activates Myosin Light Chain Kinase (MLCK) to promote actomyosin contractility and amoeboid migration. Using a microchannel based assay, we find that ROCK2 and not MLCK, promotes amoeboid migration. Altogether, our work reveals an unanticipated collaboration between Piezo1 and ROCK2 in amoeboid migrating melanoma cells. Citation Format: Alexa Caruso, Neelakshi Kar, Jeremy Logue. Piezo1 and ROCK2 promote fast amoeboid migration in confined environments [abstract]. In: Proceedings of the AACR Special Conference: Cancer Metastasis; 2022 Nov 14-17; Portland, OR. Philadelphia (PA): AACR; Cancer Res 2022;83(2 Suppl_2):Abstract nr B021.
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Vosatka, Karl W., Sandrine B. Lavenus, and Jeremy S. Logue. "A novel Fiji/ImageJ plugin for the rapid analysis of blebbing cells." PLOS ONE 17, no. 4 (April 29, 2022): e0267740. http://dx.doi.org/10.1371/journal.pone.0267740.

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When confined, cells have recently been shown to undergo a phenotypic switch to what has been termed, fast amoeboid (leader bleb-based) migration. However, as this is a nascent area of research, few tools are available for the rapid analysis of cell behavior. Here, we demonstrate that a novel Fiji/ImageJ-based plugin, Analyze_Blebs, can be used to quickly obtain cell migration parameters and morphometrics from time lapse images. As validation, we show that Analyze_Blebs can detect significant differences in cell migration and morphometrics, such as the largest bleb size, upon introducing different live markers of F-actin, including F-tractin and LifeAct tagged with green and red fluorescent proteins. We also demonstrate, using flow cytometry, that live markers increase total levels of F-actin. Furthermore, that F-tractin increases cell stiffness, which was found to correlate with a decrease in migration, thus reaffirming the importance of cell mechanics as a determinant of Leader Bleb-Based Migration (LBBM).
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Richardson, Jo, Anton Gauert, Luis Briones Montecinos, Lucía Fanlo, Zainalabdeen Mohmammed Alhashem, Rodrigo Assar, Elisa Marti, Alexandre Kabla, Steffen Härtel, and Claudia Linker. "Leader Cells Define Directionality of Trunk, but Not Cranial, Neural Crest Cell Migration." Cell Reports 15, no. 9 (May 2016): 2076–88. http://dx.doi.org/10.1016/j.celrep.2016.04.067.

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Wynn, Michelle L., Paul M. Kulesa, and Santiago Schnell. "Computational modelling of cell chain migration reveals mechanisms that sustain follow-the-leader behaviour." Journal of The Royal Society Interface 9, no. 72 (January 4, 2012): 1576–88. http://dx.doi.org/10.1098/rsif.2011.0726.

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Follow-the-leader chain migration is a striking cell migratory behaviour observed during vertebrate development, adult neurogenesis and cancer metastasis. Although cell–cell contact and extracellular matrix (ECM) cues have been proposed to promote this phenomenon, mechanisms that underlie chain migration persistence remain unclear. Here, we developed a quantitative agent-based modelling framework to test mechanistic hypotheses of chain migration persistence. We defined chain migration and its persistence based on evidence from the highly migratory neural crest model system, where cells within a chain extend and retract filopodia in short-lived cell contacts and move together as a collective. In our agent-based simulations, we began with a set of agents arranged as a chain and systematically probed the influence of model parameters to identify factors critical to the maintenance of the chain migration pattern. We discovered that chain migration persistence requires a high degree of directional bias in both lead and follower cells towards the target. Chain migration persistence was also promoted when lead cells maintained cell contact with followers, but not vice-versa. Finally, providing a path of least resistance in the ECM was not sufficient alone to drive chain persistence. Our results indicate that chain migration persistence depends on the interplay of directional cell movement and biased cell–cell contact.
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Dissertations / Theses on the topic "Leader cells in cell migration"

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Kozyrska, Katarzyna. "The mechanisms underlying mechanical cell competition and leader cell migration in mammalian epithelia." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/289434.

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Cell competition is a form of cell-cell signalling that results in the elimination of less fit cells from a tissue by their fitter counterparts. I take advantage of an established in vitro model of cell competition using Madin-Darby canine kidney (MDCK) cells to shed insight into the molecular basis of cell competition in epithelial cells. In this system, silencing of the tumour suppressor scribble (scribKD) results in a 'loser' phenotype whereby scribKD cells are specifically eliminated from the monolayer by surrounding wild-type cells. More specifically, scribKD cells are compacted into tight clones through activation of a directed, collective migration in the wild-type population: scribKD are 'mechanical losers' and delaminate and die due to an intrinsic hypersensitivity to high cell density. Remarkably, p53 activation is both necessary and sufficient for this mechanical loser cell status. I first investigate the role of E-, N-, and P-cadherin in the directed migration between scribKD and wild-type cells and in scribKD cell loser status. I show that differential expression of E-cadherin between scribKD losers and wild-type winners is required but not sufficient for directed migration and has no impact on loser cell status. I also show that elevation of neither E-cadherin nor N-cadherin is sufficient to induce directed migration or loser status, but that P-cadherin may play a role in both. I next focus on translating findings about the molecular details of competition from the scribKD set-up into a system where p53 differences alone drive the formation and elimination of mechanical losers. I show that the ROCK - P-p38 - p53 pathway activated in response to mechanical compaction in scribKD cells is conserved in p53-driven losers. In the latter part of my thesis, I characterise the directed migration observed during MDCK competition by drawing parallels to canonical leader-follower migration. Canonical leader cells emerge when epithelial sheets are wounded and, by becoming migratory, drive collective cell migration of follower cells, which results in wound closure. It was not known what confers the leader cell fate. I show that p53 and its effector p21 (and potentially other cyclin-dependent kinase inhibitors) are the key drivers of leader cell migration. I demonstrate that p53-induced leaders use the same molecular pathways that have been shown to drive leader cell migration during wound healing and, in fact, p53 and p21 are also elevated in leaders generated by wounding. Importantly, I establish that p53 activity drives efficient wound closure. Lastly, I show that leader cells are often eliminated by cell competition in the final stages of wound closure, as their elevated p53 mediates their hypersensitivity to density. The model incorporating these data proposes that cellular damage during wounding generates cells with elevated p53, which become leaders and drive wound healing, but these are then cleared once the wound is closed because their high p53 levels cause them to become mechanical losers.
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Yang, Yongliang. "Emergent Leader Cells in Collective Cell Migration in In Vitro Wound Healing Assay." Diss., The University of Arizona, 2014. http://hdl.handle.net/10150/332896.

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Collective cell migration is critical for various physiological and pathological processes. In vitro wound healing assay has been widely used to study collective cell migration due to its technical simplicity and ability of revealing the complexity of collective cell migration. This project studies the function and importance of leader cells, the cells pulling cell monolayer migrating into free space, in endothelium and skin epithelial regeneration via plasma lithography enhanced in vitro wound healing assay. Despite leader cells have been identified in in vitro wound healing assays, little is known about their regulation and function on collective cell migration. First, I investigated the role of leader cells in endothelial cell collective migration. I found that the leader cell density is positively related with the cell monolayer migration rates. Second, we used this knowledge to study the effects of arsenic treatment on skin regeneration via in vitro wound healing assay. We found that low concentration of arsenic treatment can accelerate the keratinocyte monolayer migration. We further found that arsenic affected cell migration by modulating leader cell density through Nrf2 signaling pathway. As a conclusion of these studies, we evaluated the function of leader cells in collective cell migration, and elucidated the mechanism of arsenic treatment on skin regeneration.
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Dean, Zachary S. "Collective Migration Models: Dynamic Monitoring of Leader Cells in Migratory/Invasive Disease Processes." Diss., The University of Arizona, 2015. http://hdl.handle.net/10150/560817.

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Leader cells are a fundamental biological process that have only been investigated since the early 2000s. These cells have often been observed emerging at the edge of an artificial wound in 2D epithelial cell collective invasion, created with either a mechanical scrape from a pipette tip or from the removal of a plastic, physical blocker. During migration, the moving cells maintain cell-cell contacts, an important quality of collective migration; the leader cells originate from either the first or the second row, they increase in size compared to other cells, and they establish ruffled lamellipodia. Recent studies in 3D have also shown that cells emerging from an invading collective group that also exhibit leader-like properties. Exactly how leader cells influence and interact with follower cells as well as other cells types during collective migration, however, is another matter, and is a subject of intense investigation between many different labs and researchers. The majority of leader cell research to date has involved epithelial cells, but as collective migration is implicated in many different pathogenic diseases, such as cancer and wound healing, a better understanding of leader cells in many cell types and environments will allow significant improvement to therapies and treatments for a wide variety of disease processes. In fact, more recent studies on collective migration and invasion have broadened the field to include other cell types, including mesenchymal cancer cells and fibroblasts. However, the proper technology for picking out dynamic, single cells within a moving and changing cell population over time has severely limited previous investigation into leader cell formation and influence over other cells. In line with these previous studies, we not only bring new technology capable of dynamically monitoring leader cell formation, but we propose that leader cell behavior is more than just an epithelial process, and that it is a critical physiological process in multiple cell types and diseases.
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Sharma, Puja. "A Suspended Fiber Network Platform for the Investigation of Single and Collective Cell Behavior." Diss., Virginia Tech, 2016. http://hdl.handle.net/10919/82709.

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Cells interact with their immediate fibrous extracellular matrix (ECM); alignment of which has been shown influence metastasis. Specifically, intra-vital imaging studies on cell invasion from tumor-matrix interface and wounds along aligned fibers describe invasion to occur as singular leader (tip) cells, or as collective mass of a few chain or multiple tip cells. Recapitulation of these behaviors in vitro promises to provide new insights in how, when and where cells get the stimulus to break cell-cell junctions and ensue invasion by migrating along aligned tracks. Using Spinneret based Tunable Engineered Parameters (STEP) technique, we fabricated precise layout of suspended fibers of varying diameters (300, 500 and 1000 nm) mimicking ECM dimensions, which were interfaced with cell monolayers to study invasion. We demonstrated that nanofiber diameter and their spacing were key determinants in cells to invade either as singularly, chains of few cells or multiple-chains collectively. Through time-lapse microscopy, we reported that singular cells exhibited a peculiar invasive behavior of recoiling analogous to release of a stretched rubber band; detachment speed of which was influenced with fiber diameter (250, 425 and 400 µm/hr on small, medium and large diameter fibers respectively). We found that cells initiated invasion by putting protrusion on fibers; dynamics of which we captured using a contrasting network of mismatched diameters deposited orthogonally. We found that vimentin, a key intermediate filament upregulated in cancer invasion localized within a protrusion only when the protrusion had widened at the base, signifying maturation. To develop a comprehensive picture of invasion, we also developed strategies to quantify migratory speeds and the forces exerted by cells on fibers. Finally, we extended our findings of cell invasion to report a new wound healing assay to examine gap closure. We found that gaps spanned by crosshatch network of fibers closed faster than those on parallel fibers and importantly, we reported that gaps of 375 µm or larger did not close over a 45-day period. In summary, the methods and novel findings detailed from this study can be extended to ask multiple sophisticated hypotheses in physiologically relevant phenomenon like wound healing, morphogenesis, and cancer metastasis.
Ph. D.
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Falk, Anna. "Stem cells : proliferation, differentiation, migration /." Stockholm, 2005. http://diss.kib.ki.se/2006/91-7140-497-X/.

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Eaton, Laura. "Skin dendritic cells : activation, maturation and migration." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/skin-dendritic-cells-activation-maturation-and-migration(0831ed5e-c580-406c-a404-4b1eb59b040d).html.

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Langerhans’ cells (LC) are the dendritic cells (DC) of the epidermis and, as sentinels of the immune system, act as a bridge between the innate and adaptive immune responses. When LC, and other DC, recognise an antigen or pathogen they mature and are stimulated to migrate to the lymph nodes, where they orchestrate immune responses. Pathogen derived toll-like receptor (TLR) ligands, and chemical allergens, are recognised as being potentially harmful and stimulate LC to mobilise and mature. Cytokine signals, including tumour necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-18, all induce LC migration and are required for initiating LC mobilisation in response to certain contact allergens. Subsequently, chemokines promote the migration and localisation of LC within the draining lymph nodes. Chemokines are also involved in shaping the adaptive immune response by promoting differential T cell activation, such as T helper (Th)1 or Th2 responses, which are involved in immunity against different pathogens, and also in the development of different types of chemical allergy. The hypothesis is that LC phenotype (activation, migration and chemokine production), is dependent on the nature of the challenge ligand. The murine LC-like cell line XS106 was used to investigate the response of LC following stimulation with TLR ligands and chemical allergens. In addition, LC migration in response to these stimuli was investigated in vivo and the role of TNF-α was examined using mice deficient in either one of the two TNF-α receptors; TNF-R1 or TNF-R2.XS106 cells and freshly isolated LC were associated with a selective type 2 immune response, as determined by preferential expression of type 2 associated chemokines. Furthermore, XS106 cells responded to type 2, but not to type 1, associated TLR ligands. In contrast, all of the TLR ligands tested induced the migration of LC from the epidermis in vivo. Similarly, chemical allergens failed to induce a maximal response of XS106 cells, but did induce the migration of LC in vivo. There were differences in LC migration between the two mouse strains tested, with C57/BL6 strain mice being less responsive to administration of TNF-α and the contact allergen oxazolone compared with BALB/c strain mice. However, C57/BL6 and BALB/c strain mice responded similarly after exposure to the contact allergen 2,4-dinitrochlorobenzene (DNCB). Furthermore, DNCB was able to induce LC migration in mice deficient in TNF-R2, the TNF-α receptor expressed by LC.Collectively, these data suggest a paradigm in which keratinocytes and LC in the epidermis have distinct roles in promoting type 1 and type 2 immune responses, respectively. Therefore, LC may not be activated directly by certain TLR ligands or chemical allergens that are associated with type 1 responses. Consequently the migration of LC in vivo after encounter with these stimuli may be secondary to interaction with keratinocytes, or with other skin resident cells. Together, LC and keratinocytes allow the epidermis to respond to a range of pathogens, in addition to developing the necessary type 1 and type 2 responses. Chemical allergens may have divergent cytokine signalling requirements for the induction of LC migration as, unlike other contact allergens (and other stimuli such as irritant and ultraviolet [UV]B exposure), DNCB may induce LC migration independently of TNF-α.
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Zhao, Zhiqiang. "Electric field-directed cell migration and endothelialization." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources. Restricted: no access until June 30, 2014, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=26544.

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Vanderleyden, Ine. "Follicular regulatory T cell migration and differentiation." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/288422.

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The germinal centre (GC) response is critical for generating highly effective humoral immune responses and immunological memory that forms the basis of successful immunisation. Control of the output of the GC response requires Follicular regulatory T (Tfr) cells, a subset of Foxp3+ Treg cells located within germinal centres. Tfr cells were first characterised in detail in 2011 and because of this relatively little is known about the exact role of Tfr cells within the GC, and the mechanism/s through which they exert their suppressive function. At the outset of this work, the major barrier to understanding Tfr cell biology was the lack of appropriate tools to study Tfr cells specifically, without affecting Tfh cells or other Treg cell subsets. This thesis set out to develop a strain of mice that specifically lacks Tfr cells. A unique feature of Tfr cells is their CXCR5-dependent localisation within the GC. Therefore, genetic strategies that exclude Treg cells from entering the GC are a rational approach to generating a mouse model that lacks Tfr cells. To this end, I generated a strain of mice that lacks CXCR5 on Foxp3+ Treg cells. These animals show a ~50% reduction in GC localised Tfr cells, and a GC response that is comparable to control animals. These data indicated that redundant mechanisms are involved in Treg cell homing to the GC. I identified CXCR4 as a chemokine receptor that is also highly expressed on Tfr cells, and hypothesised that it may also be involved in Tfr cell localisation to the GC. Surprisingly, simultaneous deletion of both CXCR4 and CXCR5 in Treg cells resulted in a less marked reduction in Tfr cells compared to deletion of CXCR5 alone, suggesting that CXCR4 might be involved in negative regulation of Treg homing to the GC. These data identify both CXCR4 and CXCR5 as key regulators of Tfr cell biology. Bcl6 drives Tfr cell differentiation, but how this transcriptional repressor facilitates commitment to the Tfr cell subset is unknown. I hypothesised that Bcl6 drives Tfr cell differentiation by repressing Tbx21, the transcriptional regulator involved in the differentiation of Th1-like Treg cells. I tested this hypothesis in Bcl6fl/fl CD4cre/+ animals and unexpectedly found that loss of Bcl6 regulates Treg cell differentiation in the absence of immunisation or infection. I have demonstrated that thymic loss of Bcl6 results in an increase in activated effector Treg cells, which occurs very early in life. These data point to a novel role for Bcl6 in preventing early thymic Treg activation, indicating that Bcl6 has a global role in Treg development and differentiation that is not simply limited to Tfr cells.
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Olsson, Niclas. "Mast Cell Migration in Inflammatory Diseases." Doctoral thesis, Uppsala University, Department of Genetics and Pathology, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3615.

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Mast cells (MCs) are forceful multifunctional effector cells of the immune system. MCs are normally distributed throughout connective and mucosal tissues, but in several pathological conditions accumulation of MCs occur. This accumulation is probable due to directed migration of MCs and they are subjects for migration at least two different occations: 1) when they are recruited as progenitor cells from the blood into the tissue; and 2) when they as mature MCs are recruited to sites of inflammation. The aim of this study was to investigate MC migration to chemoattractants released in vivo or in vitro (body fluids collected from patients with asthma or rheumatoid arthritis and TH1- and TH2-cytokines) and to recombinant cytokines (transforming growth factor -β (TGF-β) and CCL5/RANTES).

This thesis shows that bronchoalveolar lavage (BAL) fluid from asthmatic patients and synovial fluid from patients with rheumatiod arthritis contain MC chemoattractants, and that part of the chemotactic activity can be related to the presence of stem cell factor (SCF) and TGF-β. We also show that MC chemotactic activity during pollen season is significantly increased compared to before pollen season. Furthermore, we demonstrate that TGF-β isoforms, CCL5, TNF-α and IL-4 act as MC chemoattractants in a bellshaped dose- dependent manner. TGF-β proved to be an extremely potent attractant giving an optimal migratory response at 40fM and TGF-β3 being the most effective isoform. The chemokine CCL5 induced migration through interaction with the receptors CCR1 and CCR4 expressed on MC. Furthermore, we also found that TNF-α produced by TH1-lymphocytes and IL-4 produced by TH2-lymphocytes are MC chemoattractants.

In conclusion, with this thesis we have identified six new human mast cell chemoattractants and provide evidence that BAL fluid and synovial fluid from patients with asthma and rheumatoid arthritis, respectivly, contain MC chemoattractants. This information provides important clues in understanding the mechanisms behind MC recruitment to sites of inflammation.

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Erlandsson, Anna. "Neural Stem Cell Differentiation and Migration." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl.[distributör], 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3546.

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Books on the topic "Leader cells in cell migration"

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In vivo migration of immune cells. Boca Raton, Fla: CRC Press, 1987.

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1949-, Husband Alan J., ed. Migration and homing of lymphoid cells. Boca Raton, Fla: CRC Press, 1988.

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Stem cell migration: Methods and protocols. New York: Humana Press, 2011.

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Frank, Entschladen, and Zänker Kurt S, eds. Cell migration: Signalling and mechanisms. Basel: Karger, 2010.

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Tsai, Ching-Wei, Sanjeev Noel, and Hamid Rabb. Pathophysiology of Acute Kidney Injury, Repair, and Regeneration. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0030.

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Acute kidney injury (AKI), regardless of its aetiology, can elicit persistent or permanent kidney tissue changes that are associated with progression to end-stage renal disease and a greater risk of chronic kidney disease (CKD). In other cases, AKI may result in complete repair and restoration of normal kidney function. The pathophysiological mechanisms of renal injury and repair include vascular, tubular, and inflammatory factors. The initial injury phase is characterized by rarefaction of peritubular vessels and engagement of the immune response via Toll-like receptor binding, activation of macrophages, dendritic cells, natural killer cells, and T and B lymphocytes. During the recovery phase, cell adhesion molecules as well as cytokines and chemokines may be instrumental by directing the migration, differentiation, and proliferation of renal epithelial cells; recent data also suggest a critical role of M2 macrophage and regulatory T cell in the recovery period. Other processes contributing to renal regeneration include renal stem cells and the expression of growth hormones and trophic factors. Subtle deviations in the normal repair process can lead to maladaptive fibrotic kidney disease. Further elucidation of these mechanisms will help discover new therapeutic interventions aimed at limiting the extent of AKI and halting its progression to CKD or ESRD.
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Olszewski, Waldemar. In Vivo Migration of Immune Cells. Taylor & Francis Group, 2021.

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Filippi, Marie-Dominique, and Hartmut Geiger. Stem Cell Migration: Methods and Protocols. Humana Press, 2016.

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Okeyo, Kennedy Omondi Omondi, Hiromi Miyoshi, and Taiji Adachi. Innovative Approaches to Cell Biomechanics: From Cell Migration to On-Chip Manipulation. Springer, 2016.

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Miyoshi, Hiromi, Taiji Adachi, and Kennedy Omondi Okeyo. Innovative Approaches to Cell Biomechanics: From Cell Migration to On-Chip Manipulation. Hiromi Miyoshi Kennedy Omondi Okeyo Taiji Adachi, 2015.

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Miyoshi, Hiromi, Taiji Adachi, and Kennedy Omondi Okeyo. Innovative Approaches to Cell Biomechanics: From Cell Migration to On-Chip Manipulation. Springer, 2015.

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Book chapters on the topic "Leader cells in cell migration"

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Moissoglu, Konstadinos, Stephen J. Lockett, and Stavroula Mili. "Visualizing and Quantifying mRNA Localization at the Invasive Front of 3D Cancer Spheroids." In Cell Migration in Three Dimensions, 263–80. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2887-4_16.

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AbstractLocalization of mRNAs at the front of migrating cells is a widely used mechanism that functionally supports efficient cell movement. It is observed in single cells on two-dimensional surfaces, as well as in multicellular three-dimensional (3D) structures and in tissue in vivo. 3D multicellular cultures can reveal how the topology of the extracellular matrix and cell-cell contacts influence subcellular mRNA distributions. Here we describe a method for mRNA imaging in an inducible system of collective cancer cell invasion. MDA-MB-231 cancer cell spheroids are embedded in Matrigel, induced to invade, and processed to image mRNAs with single-molecule sensitivity. An analysis algorithm is used to quantify and compare mRNA distributions at the front of invasive leader cells. The approach can be easily adapted and applied to analyze RNA distributions in additional settings where cells polarize along a linear axis.
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Zhang, Jian, and Cynthia A. Reinhart-King. "Analysis of Energy-Driven Leader-Follower Hierarchy During Collective Cancer Cell Invasion." In Cell Migration in Three Dimensions, 247–62. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2887-4_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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Kim, Chang H. "Migration of Functionally Specialized T-Helper Cells: TFH Cells, Th17 Cells and FoxP3+ T Cells." In Cell Migration: Signalling and Mechanisms, 67–82. Basel: KARGER, 2009. http://dx.doi.org/10.1159/000274477.

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Nandagopal, Saravanan, Francis Lin, and Sam K. P. Kung. "Microfluidic-Based Live-Cell Analysis of NK Cell Migration In Vitro." In Natural Killer Cells, 75–86. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3684-7_7.

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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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Kimber, Ian, and Marie Cumberbatch. "Langerhans Cell Migration: Initiation and Regulation." In The Immune Functions of Epidermal Langerhans Cells, 103–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22497-7_7.

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Bambousková, Monika, Zuzana Rubíková, Lubica Dráberová, Pavel Dráber, and Petr Dráber. "Mast Cell Migration and Chemotaxis Assayed by Microscopy." In Basophils and Mast Cells, 293–310. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0696-4_24.

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Svoren, Martin, Elena Camerini, Merijn van Erp, Feng Wei Yang, Gert-Jan Bakker, and Katarina Wolf. "Approaches to Determine Nuclear Shape in Cells During Migration Through Collagen Matrices." In Cell Migration in Three Dimensions, 97–114. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2887-4_7.

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AbstractFibrillar collagen is an abundant extracellular matrix (ECM) component of interstitial tissues which supports the structure of many organs, including the skin and breast. Many different physiological processes, but also pathological processes such as metastatic cancer invasion, involve interstitial cell migration. Often, cell movement takes place through small ECM gaps and pores and depends upon the ability of the cell and its stiff nucleus to deform. Such nuclear deformation during cell migration may impact nuclear integrity, such as of chromatin or the nuclear envelope, and therefore the morphometric analysis of nuclear shapes can provide valuable insight into a broad variety of biological processes. Here, we describe a protocol on how to generate a cell-collagen model in vitro and how to use confocal microscopy for the static and dynamic visualization of labeled nuclei in single migratory cells. We developed, and here provide, two scripts that (Fidler, Nat Rev Cancer 3(6):453–458, 2003) enable the semi-automated and fast quantification of static single nuclear shape descriptors, such as aspect ratio or circularity, and the nuclear irregularity index that forms a combination of four distinct shape descriptors, as well as (Frantz et al., J Cell Sci 123 (Pt 24):4195–4200, 2010) a quantification of their changes over time. Finally, we provide quantitative measurements on nuclear shapes from cells that migrated through collagen either in the presence or the absence of an inhibitor of collagen degradation, showing the distinctive power of this approach. This pipeline can also be applied to cell migration studied in different assays, ranging from 3D microfluidics to migration in the living organism.
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van Boxtel, Antonius L. "Whole-Mount In Situ Hybridization for Detection of Migrating Zebrafish Endodermal Cells." In Cell Migration in Three Dimensions, 131–45. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2887-4_9.

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Conference papers on the topic "Leader cells in cell migration"

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Wood, Levi, and H. Harry Asada. "An Experimentally Tuned Dynamic Model Predicting Cell Migration for Guidance of Sprouting Endothelial Cells." In ASME 2011 Dynamic Systems and Control Conference and Bath/ASME Symposium on Fluid Power and Motion Control. ASMEDC, 2011. http://dx.doi.org/10.1115/dscc2011-6134.

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Endothelial cells (ECs) create a vascular network with a tubular structure in response to growth factors diffused into the gel and interactions with the surrounding environment. Individual cells migrate in response to all of these cues, leading to network pattern formation. This paper presents a dynamic model predicting EC sprout growth that is tuned to time-lapse experimental cell migration data obtained from microfluidic 3D culture. Simple cell migration equations with just a few parameters are formulated and a Maximum Likelihood estimator is used for estimating model parameters from experimental data. The tuned model is used to evaluate the influence of different sprout elongation rates on cell density in the sprout stalk. This quantitative modeling approach will lead to input shaping and feedback control to optimize sprouting metrics such as stalk cell density.
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Pan, Mengyun, Yongliang Yang, and Lianqing Liu. "Physical Forces Influence the Self-organization of the Leader Cell Formation During Collective Cell Migration." In 2021 IEEE 16th International Conference on Nano/Micro Engineered and Molecular Systems (NEMS). IEEE, 2021. http://dx.doi.org/10.1109/nems51815.2021.9451315.

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Rodriguez, Marita L., Sangyoon J. Han, and Nathan J. Sniadecki. "A Multi-Physics Finite Element Model of the Traction Forces in a Three-Dimensional Smooth Muscle Cell." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53944.

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Vascular smooth muscle cells (VSM) modulate cardiac output, maintain vascular pressure, and regulate blood flow via contraction. This contraction is generated by a mechanochemical interaction of actin-myosin cross-bridges within each cell and is governed by the biochemical and mechanical state of the cell [1]. When this state is disturbed, VSM cells can respond with excessive constriction (which can lead to hypertension) or weakened residual stresses (which can result in aortic aneurysms); both of which are considered to be symptoms of cardiovascular diseases [2]. Furthermore, disruption in the state of VSM cells can cause their migration into the intimal layer of the artery, which is a precursor to atherosclerosis.
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Sebastine, I. M., and D. J. Williams. "Requirements for the Manufacturing of Scaffold Biomaterial With Features at Multiple Scales." In ASME 2005 International Mechanical Engineering Congress and Exposition. ASMEDC, 2005. http://dx.doi.org/10.1115/imece2005-82515.

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Tissue engineering aims to restore the complex function of diseased tissue using cells and scaffold materials. Tissue engineering scaffolds are three-dimensional (3D) structures that assist in the tissue engineering process by providing a site for cells to attach, proliferate, differentiate and secrete an extra-cellular matrix, eventually leading cells to form a neo-tissue of predetermined, three-dimensional shape and size. For a scaffold to function effectively, it must possess the optimum structural parameters conducive to the cellular activities that lead to tissue formation; these include cell penetration and migration into the scaffold, cell attachment onto the scaffold substrate, cell spreading and proliferation and cell orientation. In vivo, cells are organized in functional tissue units that repeat on the order of 100 μm. Fine scaffold features have been shown to provide control over attachment, migration and differentiation of cells. In order to design such 3D featured constructs effectively understanding the biological response of cells across length scales from nanometer to millimeter range is crucial. Scaffold biomaterials may need to be tailored at three different length scales: nanostructure (<1μm), microstructure (<20–100μm), and macrostructure (>100μm) to produce biocompatible and biofunctional scaffolds that closely resemble the extracellular matrix (ECM) of the natural tissue environment and promote cell adhesion, attachment, spreading, orientation, rate of movement, and activation. Identification of suitable fabrication techniques for manufacturing scaffolds with the required features at multiple scales is a significant challenge. This review highlights the effect and importance of the features of scaffolds that can influence the behaviour of cells/tissue at different length scales in vitro to increase our understanding of the requirements for the manufacture of functional 3D tissue constructs.
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Lussier, Alexandre, Joseph Dvorak, Stephen Sofie, and Yves U. Idzerda. "Hydrogen Sulfide Induced Nickel Depletion of SOFC Anodes." In ASME 2008 6th International Conference on Fuel Cell Science, Engineering and Technology. ASMEDC, 2008. http://dx.doi.org/10.1115/fuelcell2008-65189.

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Our results reveal a mechanism for permanent degradation of solid oxide fuel cells (SOFCs) by which hydrogen sulfide leads to nickel migration and depletion of the anode, thereby compromising electrical conductivity and cell operation. Additionally, we find that this process is accentuated at higher temperatures and causes depletion of near surface nickel, while deeply buried or trapped nickel remains in the anode.
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Jou, Liang-Der. "Endothelial Cell Migration in Patient-Specific Models of Intracranial Aneurysm." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19027.

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Effects of wall shear stress on atherosclerotic disease are widely studied, but its effects on intracranial aneurysms are less clear. In vitro studies have demonstrated that endothelial cells (EC) go through morphological changes under abnormal wall shear stress, and these studies have also shown that abnormal wall shear stresses lead to a non-uniform EC distributions [1, 2]. Since endothelial cells play a critical role in mechanotransduction, a sub-optimal distribution of EC may affect remodeling of vessel wall.
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Singh, Tripti, Mudit Vaid, and Santosh K. Katiyar. "Abstract 2368: Reversal of epithelial to mesenchymal transition in non-small cell lung cancer cells by grape seed proanthocyanidins leads to decreased cancer cell migration." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2368.

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Baker, Brendon M., Giana Montero, and Robert L. Mauck. "Removal of Sacrificial Fibers Enhances Long Term Cell and Matrix Distribution in Aligned Nanofibrous Scaffolds." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206856.

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Given their ability to dictate initial cell alignment and subsequent matrix organization, aligned electrospun scaffolds are a fitting means for engineering fiber-reinforced, anisotropic tissues such as tendon, ligament, the knee meniscus, and the annulus fibrosus [1–3]. However, one commonly observed limitation of such scaffolds is the relatively slow infiltration rates of surface-seeded cells, where the central thicknesses of constructs cultured for 10 weeks remain devoid of cells [2]. This limitation arises from the tight packing of fibers which yields small pore sizes, thereby hampering cell migration. Towards accelerating cell ingress, we have recently reported on two-polymer composite scaffolds containing both slow eroding poly(ε-caprolactone) (PCL) fibers as well as water-soluble poly(ethylene oxide) (PEO) fibers that serve as space holders during scaffold formation [4]. Removal of these PEO fibers prior to seeding resulted in improved cell infiltration after 3 weeks, but the long term maturation of such constructs has yet to be characterized. To assess the effect of sacrificial PEO fiber content on construct growth, a triple-jet electrospinning device was employed to generate PCL/PEO scaffolds with PEO fiber fractions ranging from 0 to 60%. After seeding with mesenchymal stem cells (MSCs), constructs were clamped in custom grips to maintain strip morphology. The mechanical and biochemical maturation of constructs was assessed over 9 weeks of free swelling culture in a chemically defined medium (CDM), along with cell infiltration and matrix distribution. We hypothesized that enhanced pore size in dual-fiber constructs would lead to not only a better distribution of cells, but also larger increases in stiffness resulting from enhanced matrix production and distribution.
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Hashimoto, Shigehiro, and Hiroki Yonezawa. "Activity of Cell on Micro Stripe Ridges After Force Field Stimulation With Centrifuge." In ASME 2021 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/imece2021-66412.

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Abstract Does response of a cell depend on the history of the direction of mechanical stimulation? A mechanical force field generated by centrifugal force is applied to the scaffold plane in the present study. To control the cell direction (0, 45, 90 degrees) with respect to the tangential force, striped micro-ridges in 3 directions were machined on the scaffold surface by photolithography technique. The behavior (movement, and deformation) of each mouse myoblast after cultivation in the tangential force field for 5 hours was tracked for 10 hours by time-lapse images. Experimental results show that the velocity of each cell migration tends to increase regardless of two-dimensional projected area on the scaffold by hysteresis of exposure to tangential force field perpendicular to the longitudinal direction of the cell. The experimental results will lead to the elucidation of the effect of the direction of force stimulation on cells.
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Baker, Brendon M., Amy M. Silverstein, and Robert L. Mauck. "Engineering Dense Connective Tissues via Anisotropic Nanofibrous Scaffolds With High Sacrificial Fiber Content." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13371.

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Given their ability to dictate initial cell alignment and subsequent matrix organization, aligned electrospun scaffolds are a fitting means for engineering fiber-reinforced, anisotropic tissues such as tendon, ligament, the knee meniscus, and the annulus fibrosus [1–4]. However, one commonly observed limitation of such scaffolds is the relatively slow infiltration rates of surface-seeded cells, where the central thicknesses of constructs cultured for 10 weeks remain devoid of cells [3]. This limitation arises from the tight packing of fibers which yields small pore sizes, thereby hampering cell migration. Towards accelerating cell ingress, we have recently reported on two-polymer composite scaffolds containing both slow eroding poly(ε-caprolactone) (PCL) fibers as well as water-soluble poly(ethylene oxide) (PEO) fibers that serve as space holders during scaffold formation [5]. Removal of these PEO fibers prior to seeding resulted in improved cell infiltration after 3 weeks, but the long-term maturation of such constructs has yet to be characterized. To assess the effect of sacrificial PEO fiber content on construct growth, a triple-jet electrospinning device was employed to generate PCL/PEO scaffolds with PEO fiber fractions ranging from 0 to 60%. After seeding with human meniscus fibrochondrocytes (hMFCs), constructs were clamped in custom grips to maintain strip morphology. The mechanical and biochemical maturation of constructs was assessed over 12 weeks of free swelling culture in a chemically defined medium (CDM), along with cell infiltration and matrix distribution. We hypothesized that enhanced pore size in dual-fiber constructs would lead to not only to a better distribution of cells, but also to larger increases in stiffness resulting from enhanced matrix production and distribution.
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Reports on the topic "Leader cells in cell migration"

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Paul, Satashree. Flavivirus and its Threat. Science Repository, March 2021. http://dx.doi.org/10.31487/sr.blog.30.

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A number of studies found that the virus can activate the endothelial cells and affect the structure and function of the blood?brain barrier, promoting immune cell migration to benefit the virus nervous system target cells infected by flaviviruses.
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