Статті в журналах: "Cellular Migration"

1

Mcclay, D. "Cellular migration." Reproductive Toxicology 11, no. 2-3 (June 1997): 321–29. http://dx.doi.org/10.1016/s0890-6238(96)00215-8.

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2

Schönfisch, Birgitt, and Claude Lacoursière. "Migration in cellular automata." Physica D: Nonlinear Phenomena 103, no. 1-4 (April 1997): 537–53. http://dx.doi.org/10.1016/s0167-2789(96)00284-9.

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3

Zhao, Jieling, Youfang Cao, Luisa A. DiPietro, and Jie Liang. "Dynamic cellular finite-element method for modelling large-scale cell migration and proliferation under the control of mechanical and biochemical cues: a study of re-epithelialization." Journal of The Royal Society Interface 14, no. 129 (April 2017): 20160959. http://dx.doi.org/10.1098/rsif.2016.0959.

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Computational modelling of cells can reveal insight into the mechanisms of the important processes of tissue development. However, current cell models have limitations and are challenged to model detailed changes in cellular shapes and physical mechanics when thousands of migrating and interacting cells need to be modelled. Here we describe a novel dynamic cellular finite-element model (DyCelFEM), which accounts for changes in cellular shapes and mechanics. It also models the full range of cell motion, from movements of individual cells to collective cell migrations. The transmission of mechanical forces regulated by intercellular adhesions and their ruptures are also accounted for. Intra-cellular protein signalling networks controlling cell behaviours are embedded in individual cells. We employ DyCelFEM to examine specific effects of biochemical and mechanical cues in regulating cell migration and proliferation, and in controlling tissue patterning using a simplified re-epithelialization model of wound tissue. Our results suggest that biochemical cues are better at guiding cell migration with improved directionality and persistence, while mechanical cues are better at coordinating collective cell migration. Overall, DyCelFEM can be used to study developmental processes when a large population of migrating cells under mechanical and biochemical controls experience complex changes in cell shapes and mechanics.

4

Kravets, E. A., A. I. Yemets, and Ya B. Blume. "Cellular mechanisms of nuclear migration." Cytology and Genetics 51, no. 3 (May 2017): 192–201. http://dx.doi.org/10.3103/s0095452717030069.

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5

Vaughan, Douglas E. "PAI-1 and Cellular Migration." Arteriosclerosis, Thrombosis, and Vascular Biology 22, no. 10 (October 2002): 1522–23. http://dx.doi.org/10.1161/01.atv.0000037901.89736.0a.

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6

Chang, Stephanie S., Andrew D. Rape, Stephanie A. Wong, Wei-hui Guo, and Yu-li Wang. "Migration regulates cellular mechanical states." Molecular Biology of the Cell 30, no. 26 (December 15, 2019): 3104–11. http://dx.doi.org/10.1091/mbc.e19-02-0099.

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Cell migration has a profound effect on the generation of traction forces and the phosphorylation of focal adhesion proteins. The mechanism may involve the dynamic turnover of focal adhesions during cell migration and mechanical interactions between nascent and preexisting focal adhesions.

7

Verdoorn, Cornelis. "Cellular Migration, Proliferation, and Contraction." Archives of Ophthalmology 104, no. 8 (August 1, 1986): 1216. http://dx.doi.org/10.1001/archopht.1986.01050200122064.

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8

Nagayama, M., H. Haga, M. Takahashi, and K. Kawabata. "Cellular migration coordinated by cortical tension." Seibutsu Butsuri 43, supplement (2003): S108. http://dx.doi.org/10.2142/biophys.43.s108_3.

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9

SCHUBERT, THOMAS, ALEXANDRA E. DENK, ANKE RUEDEL, SIMONE KAUFMANN, ELISABETH HUSTERT, PATRIZIA BASTONE, and ANJA K. BOSSERHOFF. "Fragments of SLIT3 inhibit cellular migration." International Journal of Molecular Medicine 30, no. 5 (August 20, 2012): 1133–37. http://dx.doi.org/10.3892/ijmm.2012.1098.

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10

Reyes-Aldasoro, C. C., D. Biram, G. M. Tozer, and C. Kanthou. "Measuring cellular migration with image processing." Electronics Letters 44, no. 13 (2008): 791. http://dx.doi.org/10.1049/el:20080943.

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11

Hisatomi, Toshio. "Cellular Migration Associated With Macular Hole." Archives of Ophthalmology 124, no. 7 (July 1, 2006): 1005. http://dx.doi.org/10.1001/archopht.124.7.1005.

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12

Quiñones, Gabriel A., and Anthony E. Oro. "BAR domain competition during directional cellular migration." Cell Cycle 9, no. 13 (July 2010): 2522–28. http://dx.doi.org/10.4161/cc.9.13.12123.

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13

Jones, Gareth E. "Cellular signaling in macrophage migration and chemotaxis." Journal of Leukocyte Biology 68, no. 5 (November 2000): 593–602. http://dx.doi.org/10.1189/jlb.68.5.593.

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14

Guck, Jochen, Franziska Lautenschläger, Stephan Paschke, and Michael Beil. "Critical review: cellular mechanobiology and amoeboid migration." Integrative Biology 2, no. 11-12 (September 27, 2010): 575–83. http://dx.doi.org/10.1039/c0ib00050g.

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15

Olsen, Abby L., and Rebecca G. Wells. "Cellular fibronectin enhances hepatic stellate cell migration." Matrix Biology 27 (December 2008): 46. http://dx.doi.org/10.1016/j.matbio.2008.09.365.

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16

Ariano, P., C. Distasi, A. Gilardino, P. Zamburlin, and M. Ferraro. "A simple method to study cellular migration." Journal of Neuroscience Methods 141, no. 2 (February 2005): 271–76. http://dx.doi.org/10.1016/j.jneumeth.2004.07.001.

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17

Recklies, Anneliese D. "Biochemical aspects of cellular migration and invasion." Biorheology 24, no. 2 (April 1, 1987): 93–103. http://dx.doi.org/10.3233/bir-1987-24203.

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18

Yamao, Masataka, Honda Naoki, and Shin Ishii. "Multi-Cellular Logistics of Collective Cell Migration." PLoS ONE 6, no. 12 (December 21, 2011): e27950. http://dx.doi.org/10.1371/journal.pone.0027950.

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19

PARK, A., T. DEWERS, and P. ORTOLEVA. "Cellular and oscillatory self-induced methane migration." Earth-Science Reviews 29, no. 1-4 (October 1990): 249–65. http://dx.doi.org/10.1016/0012-8252(0)90041-s.

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20

Park, A. "Cellular and oscillatory self-induced methane migration." Earth-Science Reviews 29, no. 1-4 (October 1990): 249–65. http://dx.doi.org/10.1016/0012-8252(90)90041-s.

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21

Willett, Mark, Michele Brocard, Alexandre Davide, and Simon J. Morley. "Translation initiation factors and active sites of protein synthesis co-localize at the leading edge of migrating fibroblasts." Biochemical Journal 438, no. 1 (July 27, 2011): 217–27. http://dx.doi.org/10.1042/bj20110435.

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Анотація:

Cell migration is a highly controlled essential cellular process, often dysregulated in tumour cells, dynamically controlled by the architecture of the cell. Studies involving cellular fractionation and microarray profiling have previously identified functionally distinct mRNA populations specific to cellular organelles and architectural compartments. However, the interaction between the translational machinery itself and cellular structures is relatively unexplored. To help understand the role for the compartmentalization and localized protein synthesis in cell migration, we have used scanning confocal microscopy, immunofluorescence and a novel ribopuromycylation method to visualize translating ribosomes. In the present study we show that eIFs (eukaryotic initiation factors) localize to the leading edge of migrating MRC5 fibroblasts in a process dependent on TGN (trans-Golgi network) to plasma membrane vesicle transport. We show that eIF4E and eIF4GI are associated with the Golgi apparatus and membrane microdomains, and that a proportion of these proteins co-localize to sites of active translation at the leading edge of migrating cells.

22

SHMIDT, Yurii D., Natal'ya V. IVASHINA, and Galina P. OZEROVA. "Forecasting interregional youth migration flows." Regional Economics: Theory and Practice 20, no. 2 (February 15, 2022): 329–54. http://dx.doi.org/10.24891/re.20.2.329.

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Subject. This article deals with the issues of youth migration, reproduction processes and the potential for the future socio-economic development of areas. Objectives. The article aims to develop a cellular automata model for the medium-term prediction of inter-regional youth migration flows of the 15–19 age cohort. Methods. For the study, we used a statistical analysis and the cellular automata theory. Results. The article presents a probabilistic cellular automata model with rectangular grids of cells without borders, where the number of cells coincides with the 15–19 age cohort number in the respective area. The article also proposes an author-developed cross-platform program in the Go programming language that helps make medium-term forecasts. Conclusions. The cellular automata allow for integrating various patterns of migratory behavior into a general model of area migration flow, and choosing the most adequate patterns of migratory behavior for various age and social groups of migrants.

23

Ridley, Anne J. "Rho GTPases and cell migration." Journal of Cell Science 114, no. 15 (August 1, 2001): 2713–22. http://dx.doi.org/10.1242/jcs.114.15.2713.

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Cell migration involves dynamic and spatially regulated changes to the cytoskeleton and cell adhesion. The Rho GTPases play key roles in coordinating the cellular responses required for cell migration. Recent research has revealed new molecular links between Rho family proteins and the actin cytoskeleton, showing that they act to regulate actin polymerization, depolymerization and the activity of actin-associated myosins. In addition, studies on integrin signalling suggest that the substratum continuously feeds signals to Rho proteins in migrating cells to influence migration rate. There is also increasing evidence that Rho proteins affect the organization of the microtubule and intermediate filament networks and that this is important for cell migration.

24

McKenzie, Andrew J., Kathryn V. Svec, Tamara F. Williams, and Alan K. Howe. "Protein kinase A activity is regulated by actomyosin contractility during cell migration and is required for durotaxis." Molecular Biology of the Cell 31, no. 1 (January 1, 2020): 45–58. http://dx.doi.org/10.1091/mbc.e19-03-0131.

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Here, we show that localized PKA activity in migrating cells is regulated by cell–matrix tension, correlates with cellular traction forces, is enhanced by acute mechanical stimulation, and is required for durotaxis. This establishes PKA as an effector of cellular mechanotransduction and as a regulator of mechanically guided cell migration.

25

Austin, C. P., and C. L. Cepko. "Cellular migration patterns in the developing mouse cerebral cortex." Development 110, no. 3 (November 1, 1990): 713–32. http://dx.doi.org/10.1242/dev.110.3.713.

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The migration patterns of embryonic mouse cortical cells were investigated using a replication-incompetent retrovirus vector (BAG). The lateral ventricles of embryonic day 12 mouse embryos were infected with BAG and brains were harvested 2, 3, 4 and 6 days after infection. The location and morphology of all infected cortical cells were recorded from serial sections of entire brains, which were then reconstructed in three dimensions. Examination of the distribution of labelled cells revealed that there were migration patterns characteristic of each medial-lateral domain of the cortex. In the medial and dorsal areas, migration was often radial, although tangential spread increased with survival time, in large part due to ramification of cells in the intermediate zone. In the dorsolateral and lateral areas of the cortex, radial migration was generally not observed. Rather, variable extents of tangential migration occurred, and often resulted in wide separation of cells in the cortical plate. Almost all of the cellular dispersion occurred in the intermediate zone, although a modest degree of dispersion also occurred within the cortical plate itself. Most dispersion occurred in the mediolateral plane, with relatively little dispersion along the anteroposterior axis. Though characteristic migration patterns could be defined, wide variability in the extents of radial migration and tangential separation of cells was seen. The patterns of migration paralleled the distribution of radial glial fibers in all areas, and are most likely a reflection of the role of this network in supporting the migration of cortical neurons. The extent and variability of cellular dispersion supports a lineage-independent mechanism of cortical column ontogenesis.

26

Augustin-Voss, H. G., and B. U. Pauli. "Migrating endothelial cells are distinctly hyperglycosylated and express specific migration-associated cell surface glycoproteins." Journal of Cell Biology 119, no. 2 (October 15, 1992): 483–91. http://dx.doi.org/10.1083/jcb.119.2.483.

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Migration of endothelial cells is one of the first cellular responses in the cascade of events that leads to re-endothelialization of an injured vessel and neovascularization of growing tissues and tumors. To examine the hypothesis that endothelial cells express a specific migration-associated phenotype, we analyzed the cell surface glycoprotein expression of migrating bovine aortic endothelial cell (BAECs). Light microscopic analysis revealed an upregulation of binding sites for the lectins Concanavalin A (Con A), wheat germ agglutinin (WGA), and peanut agglutinin after neuraminidase treatment (N-PNA) on migrating endothelial cells relative to contact-inhibited cells. These findings were confirmed and quantitated with an enzyme-linked lectin assay (ELLA) of circularly scraped BAEC monolayers. The expression of migration-associated cell surface glycoproteins was also analyzed by SDS-PAGE. The overall expression of cell surface glycoproteins was upregulated on migrating BAECs. Migrating BAECs expressed Con A- and WGA-binding glycoproteins with apparent molecular masses of 25 and 48 kD that were not expressed by contact-inhibited BAEC monolayers and, accordingly, disappeared as circularly scraped monolayers reached confluence. Subconfluent BAEC monolayers expressed the same cell surface glycoconjugate pattern as migrating endothelial cells. FACS analysis of circularly scraped BAEC monolayers showed that the phenotypic changes of cell surface glycoprotein expression after release from growth arrest occurred before the recruitment of the cells into the cell cycle (3 vs. 12 h). Suramin, which inhibits endothelial cell migration, abrogated the expression of the migration-associated phenotype and induced the expression of a prominent 28-kD Con A- and WGA-binding cell surface glycoprotein. These results indicate that endothelial cells express a specific migration-associated phenotype, which is characterized by the upregulation of distinct cellular glycoconjugates and the expression of specific migration-associated cell surface glycoproteins.

27

Bokhobza, Alexandre, Nathalie Ziental-Gelus, Laurent Allart, Oksana Iamshanova, and Fabien Vanden Abeele. "Impact of SOCE Abolition by ORAI1 Knockout on the Proliferation, Adhesion, and Migration of HEK-293 Cells." Cells 10, no. 11 (November 4, 2021): 3016. http://dx.doi.org/10.3390/cells10113016.

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Store-operated calcium entry (SOCE) provided through channels formed by ORAI proteins is a major regulator of several cellular processes. In immune cells, it controls fundamental processes such as proliferation, cell adhesion, and migration, while in cancer, SOCE and ORAI1 gene expression are dysregulated and lead to abnormal migration and/or cell proliferation. In the present study, we used the CRISPR/Cas9 technique to delete the ORAI1 gene and to identify its role in proliferative and migrative properties of the model cell line HEK-293. We showed that ORAI1 deletion greatly reduced SOCE. Thereby, we found that this decrease and the absence of ORAI1 protein did not affect HEK-293 proliferation. In addition, we determined that ORAI1 suppression did not affect adhesive properties but had a limited impact on HEK-293 migration. Overall, we showed that ORAI1 and SOCE are largely dispensable for cellular proliferation, migration, and cellular adhesion of HEK-293 cells. Thus, despite its importance in providing Ca2+ entry in non-excitable cells, our results indicate that the lack of SOCE does not deeply impact HEK-293 cells. This finding suggests the existence of compensatory mechanism enabling the maintenance of their physiological function.

28

Savino, W., S. Ayres Martins, S. Neves-dos-Santos, S. Smaniotto, J. S. P. Ocampo, D. A. Mendes-da-Cruz, E. Terra-Granado, O. Kusmenok, and D. M. S. Villa-Verde. "Thymocyte migration: an affair of multiple cellular interactions?" Brazilian Journal of Medical and Biological Research 36, no. 8 (August 2003): 1015–25. http://dx.doi.org/10.1590/s0100-879x2003000800007.

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29

Szabo, Eva, Sylvia Papp, and Michal Opas. "Calreticulin and cellular adhesion/migration-specific signalling pathways." Journal of Applied Biomedicine 4, no. 1 (March 31, 2006): 45–52. http://dx.doi.org/10.32725/jab.2006.003.

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30

Shmidt, Yuriy Davidovich, Natalya Victorovna Ivashina, and Galina Pavlovna Ozerova. "Modelling interregional migration flows by the cellular automata." Computer Research and Modeling 12, no. 6 (December 2020): 1467–83. http://dx.doi.org/10.20537/2076-7633-2020-12-6-1467-1483.

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31

Girard, Nadine J., and Charles A. Raybaud. "In Vivo MRI of Fetal Brain Cellular Migration." Journal of Computer Assisted Tomography 16, no. 2 (March 1992): 265–67. http://dx.doi.org/10.1097/00004728-199203000-00016.

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32

Cao, Di, Wai Kit Chu, Tsz Kin Ng, Yolanda W. Y. Yip, Alvin L. Young, Chi Pui Pang, and Vishal Jhanji. "Cellular Proliferation and Migration of Human Pterygium Cells." Cornea 37, no. 6 (June 2018): 760–66. http://dx.doi.org/10.1097/ico.0000000000001569.

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33

Li, Zhiping, Xuanmao Jiao, Chenguang Wang, Xiaoming Ju, Yinan Lu, Liangping Yuan, Michael P. Lisanti, Sanjay Katiyar, and Richard G. Pestell. "Cyclin D1 Induction of Cellular Migration Requires p27KIP1." Cancer Research 66, no. 20 (October 15, 2006): 9986–94. http://dx.doi.org/10.1158/0008-5472.can-06-1596.

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34

Tay, Chor Yong, Pingqiang Cai, Magdiel I. Setyawati, Wanru Fang, Lay Poh Tan, Catherine H. L. Hong, Xiaodong Chen, and David Tai Leong. "Nanoparticles Strengthen Intracellular Tension and Retard Cellular Migration." Nano Letters 14, no. 1 (December 18, 2013): 83–88. http://dx.doi.org/10.1021/nl4032549.

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35

Wismayer, K., N. Mehrban, J. Bowen, and M. Birchall. "Improving cellular migration in tissue-engineered laryngeal scaffolds." Journal of Laryngology & Otology 133, no. 2 (February 2019): 135–48. http://dx.doi.org/10.1017/s0022215119000082.

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AbstractObjectiveTo modify the non-porous surface membrane of a tissue-engineered laryngeal scaffold to allow effective cell entry.MethodsThe mechanical properties, surface topography and chemistry of polyhedral oligomeric silsesquioxane poly(carbonate-urea) urethane were characterised. A laser technique introduced surface perforations. Micro computed tomography generated porosity data. Scaffolds were seeded with cells, investigated histologically and proliferation studied. Incubation and time effects were assessed.ResultsLaser cutting perforated the polymer, connecting the substructure with the ex-scaffold environment and increasing porosity (porous, non-perforated = 87.9 per cent; porous, laser-perforated at intensities 3 = 96.4 per cent and 6 = 89.5 per cent). Cellular studies confirmed improved cell viability. Histology showed cells adherent to the scaffold surface and cells within perforations, and indicated that cells migrated into the scaffolds. After 15 days of incubation, scanning electron microscopy revealed an 11 per cent reduction in pore diameter, correlating with a decrease in Young's modulus.ConclusionIntroducing surface perforations presents a viable method of improving polyhedral oligomeric silsesquioxane poly(carbonate-urea) urethane as a tissue-engineered scaffold.

36

Trepat, Xavier, and Jeffrey J. Fredberg. "Plithotaxis and emergent dynamics in collective cellular migration." Trends in Cell Biology 21, no. 11 (November 2011): 638–46. http://dx.doi.org/10.1016/j.tcb.2011.06.006.

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37

Carman, Christopher V., and Timothy A. Springer. "Trans-cellular migration: cell–cell contacts get intimate." Current Opinion in Cell Biology 20, no. 5 (October 2008): 533–40. http://dx.doi.org/10.1016/j.ceb.2008.05.007.

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38

Guak, Hannah, and Connie M. Krawczyk. "Implications of cellular metabolism for immune cell migration." Immunology 161, no. 3 (September 29, 2020): 200–208. http://dx.doi.org/10.1111/imm.13260.

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39

Fujikura, Kie, Akiko Obata, and Toshihiro Kasuga. "Cellular Migration to Electrospun Poly(Lactic Acid) Fibermats." Journal of Biomaterials Science, Polymer Edition 23, no. 15 (May 8, 2012): 1939–50. http://dx.doi.org/10.1163/092050611x599328.

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40

Morita, Noriyuki, Kazuhiro Ikenaka, Ichiro Fujino, Masaharu Ogawa, and Katsuhiko Mikoshiba. "Cellular migration in cerebral cortex slices in vitro." Neuroscience Research Supplements 15 (January 1990): S30. http://dx.doi.org/10.1016/0921-8696(90)90119-n.

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41

Morita, Noriyuki, Kazuhiro Ikenaka, Ichiro Fujino, Masaharu Ogawa, and Katsuhiko Mikoshiba. "Cellular migration in cerebral cortex slices in vitro." Neuroscience Research Supplements 11 (January 1990): S30. http://dx.doi.org/10.1016/0921-8696(90)90542-b.

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42

Cheng, Hong, Xin Zhang, and Yinmou Li. "Hydroxycamptothecin Impedes the Mesenchymal Stem Cells (MSCs)-Triggered Migrative Features of Breast Cancer Cells via Suppressing the Protein Kinase B/Mitogen-Activated Protein Kinase (AKT/MAPK) Activation in Bone Marrowmesenchymal Stem Cells." Journal of Biomaterials and Tissue Engineering 12, no. 2 (February 1, 2022): 432–38. http://dx.doi.org/10.1166/jbt.2022.2892.

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The current study aimed to dissect the impacts and mechanisms of hydroxycamptothecin on breast cancer. Collect conditioned medium from MSCs cells to apply it into the co-culture system of breast cancer cells, which were pre-treated with hydroxycamptothecin. The cell counting kit was employed to measure the proliferation potential of cells, while the phosphorylation degrees of AKT/MAPKrelated proteins were examined via Western blotting. Then the cellular migration was test by transwell. Finally, the transcriptional and translational levels of IL-6 and RANTES in cells were detected by real-time PCR and enzyme-linked immunosorbent assay. HC could remarkably influence the interplay between MSC and breast malignant cells, reduce the MSC-activated migrative behavior of breast malignant cells and impede the capability of MSC to maintain the migration of cancer cells. RANTES and IL-6 exerted a synergistic induction in the migrative feature of breast cancer cells. HC could retard the migrating activities of breast cancer cells via diminishing the RANTES and IL-6 levels. Hydroxycamptothecin could impede the proliferative and migrative activities of MSC, of which the impediment was accompanied by an inhibitory impact on the secretory production of two growth factors IL-6 and RANTES from MSC, thereby enhancing the migration of breast malignant cells.

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Kim, Sarah Hyun Ji, and Daniel A. Hammer. "Integrin crosstalk allows CD4+ T lymphocytes to continue migrating in the upstream direction after flow." Integrative Biology 11, no. 10 (October 2019): 384–93. http://dx.doi.org/10.1093/intbio/zyz034.

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Abstract In order to perform critical immune functions at sites of inflammation, circulatory T lymphocytes must be able to arrest, adhere, migrate and transmigrate on the endothelial surface. This progression of steps is coordinated by cellular adhesion molecules (CAMs), chemokines, and selectins presented on the endothelium. Two important interactions are between Lymphocyte Function-associated Antigen-1 (LFA-1) and Intracellular Adhesion Molecule-1 (ICAM-1) and also between Very Late Antigen-4 (VLA-4) and Vascular Cell Adhesion Molecule-1 (VCAM-1). Recent studies have shown that T lymphocytes and other cell types can migrate upstream (against the direction) of flow through the binding of LFA-1 to ICAM-1. Since upstream migration of T cells depends on a specific adhesive pathway, we hypothesized that mechanotransduction is critical to migration, and that signals might allow T-cells to remember their direction of migration after the flow is terminated. Cells on ICAM-1 surfaces migrate against the shear flow, but the upstream migration reverts to random migration after the flow is stopped. Cells on VCAM-1 migrate with the direction of flow. However, on surfaces that combine ICAM-1 and VCAM-1, cells crawl upstream at a shear rate of 800 s−1 and continue migrating in the upstream direction for at least 30 minutes after the flow is terminated—we call this ‘migrational memory’. Post-flow upstream migration on VCAM-1/ICAM-1 surfaces is reversed upon the inhibition of PI3K, but conserved with cdc42 and Arp2/3 inhibitors. Using an antibody against VLA-4, we can block migrational memory on VCAM-1/ICAM-1 surfaces. Using a soluble ligand for VLA-4 (sVCAM-1), we can promote migrational memory on ICAM-1 surfaces. These results indicate that, while upstream migration under flow requires LFA-1 binding to immobilized ICAM-1, signaling from VLA-4 and PI3K activity is required for the migrational memory of CD4+ T cells. These results indicate that crosstalk between integrins potentiates the signal of upstream migration.

44

Hu, Zunlu, Jie Feng, Weijuan Bo, Ronghua Wu, Zhangji Dong, Yan Liu, Liang Qiang, and Mei Liu. "Fidgetin regulates cultured astrocyte migration by severing tyrosinated microtubules at the leading edge." Molecular Biology of the Cell 28, no. 4 (February 15, 2017): 545–53. http://dx.doi.org/10.1091/mbc.e16-09-0628.

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Microtubule (MT) organization is essential for many cellular events, including mitosis, migration, and cell polarity. Fidgetin (Fign), an ATP-dependent, MT-severing protein, contributes to the regulation of MT configuration by cutting and trimming MT polymers. Functions of Fign have been indicated in neurite outgrowth, mitosis, meiosis, and cellular migration. Here we focus on migration of astrocytes. We find that Fign plays an essential role in cultured astrocyte migration by preferentially targeting MTs (or regions of MTs) that are rich in tyrosinated tubulin, a marker for especially dynamic MTs or especially dynamic regions of MTs. Inhibition of cellular migration induced by Fign knockdown can be rescued with concomitant knockdown of kinesin-12, a motor protein best known for its role in mitosis. We propose a novel working model for MT reconfiguration underlying cellular migration elicited by the functional cooperation of two distinct MT-related proteins.

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Wang, Shuzhong, Xuzhao Li, Qianru Zhang, Xuejun Chai, Yi Wang, Eckart Förster, Xiaoyan Zhu, and Shanting Zhao. "Nyap1 Regulates Multipolar–Bipolar Transition and Morphology of Migrating Neurons by Fyn Phosphorylation during Corticogenesis." Cerebral Cortex 30, no. 3 (October 14, 2019): 929–41. http://dx.doi.org/10.1093/cercor/bhz137.

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Abstract The coordination of cytoskeletal regulation is a prerequisite for proper neuronal migration during mammalian corticogenesis. Neuronal tyrosine-phosphorylated adaptor for the phosphoinositide 3-kinase 1 (Nyap1) is a member of the Nyap family of phosphoproteins, which has been studied in neuronal morphogenesis and is involved in remodeling of the actin cytoskeleton. However, the precise role of Nyap1 in neuronal migration remains unknown. Here, overexpression and knockdown of Nyap1 in the embryonic neocortex of mouse by in utero electroporation-induced abnormal morphologies and multipolar–bipolar transitions of migrating neurons. The level of phosphorylated Nyap1 was crucial for neuronal migration and morphogenesis in neurons. Furthermore, Nyap1 regulated neuronal migration as a downstream target of Fyn, a nonreceptor protein-tyrosine kinase that is a member of the Src family of kinases. Importantly, Nyap1 mediated the role of Fyn in the multipolar–bipolar transition of migrating neurons. Taken together, these results suggest that cortical radial migration is regulated by a molecular hierarchy of Fyn via Nyap1.

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Jaglarz, M. K., and K. R. Howard. "The active migration of Drosophila primordial germ cells." Development 121, no. 11 (November 1, 1995): 3495–503. http://dx.doi.org/10.1242/dev.121.11.3495.

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We describe our analysis of primordial germ cell migration in Drosophila wild-type and mutant embryos using high resolution microscopy and primary culture in vitro. During migratory events the germ cells form transient interactions with each other and surrounding somatic cells. Both in vivo and in vitro they extend pseudopodia and the accompanying changes in the cytoskeleton suggest that actin polymerization drives these movements. These cellular events occur from the end of the blastoderm stage and are regulated by environmental cues. We show that the vital transepithelial migration allowing exit from the gut primordium and passage into the interior of the embryo is facilitated by changes in the structure of this epithelium. Migrating germ cells extend processes in different directions. This phenomenon also occurs in primary culture where the cells move in an unoriented fashion at substratum concentration-dependent rates. In vivo this migration is oriented leading germ cells to the gonadal mesoderm. We suggest that this guidance involves stabilization of states of an intrinsic cellular oscillator resulting in cell polarization and oriented movement.

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Komatsu, Satoshi, and Mitsuo Ikebe. "ZIPK is critical for the motility and contractility of VSMCs through the regulation of nonmuscle myosin II isoforms." American Journal of Physiology-Heart and Circulatory Physiology 306, no. 9 (May 1, 2014): H1275—H1286. http://dx.doi.org/10.1152/ajpheart.00289.2013.

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Migration of medial vascular smooth muscle cells (VSMCs) into the intimal layer contributes to pathological remodeling of the blood vessel in arterial hypertension and atherosclerosis. It is well established that reorganization of cytoskeletal networks is an essential component of cellular motile events. However, there is currently a lack of insight into the cellular characteristics of VSMC migration under three-dimensional environments. Here, we investigated the mechanisms of VSMC migration and remodeling using two different collagen matrix assays as in vitro models: migration of VSMCs within a collagen matrix for VSMC invasion and contraction of a collagen gel by VSMCs for VSMC remodeling and contraction. We found that nonmuscle myosin IIA (NMIIA) and nonmuscle myosin IIB (NMIIB) differentially contribute to the migratory capacity of VSMCs via NMII isoform-dependent cytoskeletal reorganization. Depletion of NMIIA by short hairpin RNA revealed a unique interplay between actomyosin and microtubules during VSMC migration. On the other hand, NMIIB was required for the structural maintenance of migrating VSMC. Interestingly, there was a significant difference between NMIIA and NMIIB knockdown in the VSMC migration but not in the VSMC-mediated collagen gel contraction. Furthermore, depletion of zipper-interacting protein kinase by short hairpin RNA resulted in an impairment of VSMC migration and a substantial decrease of VSMC-mediated collagen gel contraction. These results suggest that NMIIA and NMIIB uniquely control VSMC migration and may contribute to vascular remodeling, which are both regulated by zipper-interacting protein kinase.

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Sala, Federico, Carlotta Ficorella, Roberto Osellame, Josef A. Käs, and Rebeca Martínez Vázquez. "Microfluidic Lab-on-a-Chip for Studies of Cell Migration under Spatial Confinement." Biosensors 12, no. 8 (August 5, 2022): 604. http://dx.doi.org/10.3390/bios12080604.

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Understanding cell migration is a key step in unraveling many physiological phenomena and predicting several pathologies, such as cancer metastasis. In particular, confinement has been proven to be a key factor in the cellular migration strategy choice. As our insight in the field improves, new tools are needed in order to empower biologists’ analysis capabilities. In this framework, microfluidic devices have been used to engineer the mechanical and spatial stimuli and to investigate cellular migration response in a more controlled way. In this work, we will review the existing technologies employed in the realization of microfluidic cellular migration assays, namely the soft lithography of PDMS and hydrogels and femtosecond laser micromachining. We will give an overview of the state of the art of these devices, focusing on the different geometrical configurations that have been exploited to study specific aspects of cellular migration. Our scope is to highlight the advantages and possibilities given by each approach and to envisage the future developments in in vitro migration studies under spatial confinement in microfluidic devices.

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Fracchia, Andrea, Tal Asraf, Mali Salmon-Divon, and Gabi Gerlitz. "Increased Lamin B1 Levels Promote Cell Migration by Altering Perinuclear Actin Organization." Cells 9, no. 10 (September 24, 2020): 2161. http://dx.doi.org/10.3390/cells9102161.

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Cell migration requires reposition and reshaping of the cell nucleus. The nuclear lamina is highly important for migration of both primary and cancer cells. B-type lamins are important for proper migration of epicardial cells and neurons and increased lamin B to lamin A ratio accelerates cancer cell migration through confined spaces. Moreover, a positive association between lamin B1 levels and tumor formation and progression is found in various cancer types. Still, the molecular mechanism by which B-type lamins promote cell migration is not fully understood. To better understand this mechanism, we tested the effects of lamin B1 on perinuclear actin organization. Here we show that induction of melanoma cell migration leads to the formation of a cytosolic Linker of Nucleoskeleton and Cytoskeleton (LINC) complex-independent perinuclear actin rim, which has not been detected in migrating cells, yet. Significantly, increasing the levels of lamin B1 but not the levels of lamin A prevented perinuclear actin rim formation while accelerated the cellular migration rate. To interfere with the perinuclear actin rim, we generated a chimeric protein that is localized to the outer nuclear membrane and cleaves perinuclear actin filaments in a specific manner without disrupting other cytosolic actin filaments. Using this tool, we found that disruption of the perinuclear actin rim accelerated the cellular migration rate in a similar manner to lamin B1 over-expression. Taken together, our results suggest that increased lamin B1 levels can accelerate cell migration by inhibiting the association of the nuclear envelope with actin filaments that may reduce nuclear movement and deformability.

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Jang, Dong Gil, Keun Yeong Kwon, Eun Kyung Song та Tae Joo Park. "Integrin β-like 1 protein (ITGBL1) promotes cell migration by preferentially inhibiting integrin-ECM binding at the trailing edge". Genes & Genomics 44, № 4 (23 січня 2022): 405–13. http://dx.doi.org/10.1007/s13258-021-01204-x.

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Abstract Background Cell migration is a basic cellular behavior involved in multiple phenomena in the human body such as embryonic development, wound healing, immune reactions, and cancer metastasis. For proper cell migration, integrin and the ECM binding complex must be disassembled for the retraction of trailing edges. Objective Integrin must be differentially regulated at leading edges or trailing edges during cell migration. Previously, we showed that ITGBL1 was a secreted protein and inhibits integrin activity. Therefore, we examined the function of ITGBL1 on the retraction of trailing edges during cell migration. Methods To examined the function of ITGBL1 on cell migration, we knocked-down or overexpressed ITGBL1 by using ITGBL1 siRNA or ITGBL1 plasmid DNA in human chondrocytes or ATDC5 cells. We then characterized cellular migration and directionality by performing wound healing assays. Also, to analyze leading-edge formation and trailing-edge retraction, we labeled cell membranes with membrane-GFP and performed live imaging of migrating cells and. Finally, we specifically detected active forms of integrin, FAK and Vinculin using specific antibodies upon ITGBL1 depletion or overexpression. Result In this study, ITGBL1 preferentially inhibited integrin activity at the trailing edges to promote cell migration. ITGBL1-depleted cells showed increased focal adhesions at the membranous traces of trailing edges to prevent the retraction of trailing edges. In contrast, overexpression of ITGBL1 upregulated directional cell migration by promoting focal adhesion disassembly at the trailing edges. Conclusion ITGBL1 facilitates directional cell migration by promoting disassembly of the trailing edge focal adhesion complex.

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