To see the other types of publications on this topic, follow the link: Tissue-specific migration.
Journal articles on the topic 'Tissue-specific migration'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Tissue-specific migration.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Kunkel, Eric J., and Eugene C. Butcher. "Chemokines and the Tissue-Specific Migration of Lymphocytes." Immunity 16, no. 1 (January 2002): 1–4. http://dx.doi.org/10.1016/s1074-7613(01)00261-8.
Full text
2
Newsome, Seth D., Pablo Sabat, Nathan Wolf, Jonathan A. Rader, and Carlos Martinez del Rio. "Multi-tissue δ2H analysis reveals altitudinal migration and tissue-specific discrimination patterns inCinclodes." Ecosphere 6, no. 11 (November 2015): art213. http://dx.doi.org/10.1890/es15-00086.1.
Full text
3
MARUYAMA, H., A. NISHIMAKI, Y. TAKUMA, M. KURIMOTO, T. SUZUKI, Y. SAKATOKU, M. ISHIKAWA, and N. OHTA. "Successive changes in tissue migration capacity of developing larvae of an intestinal nematode,Strongyloides venezuelensis." Parasitology 132, no. 3 (November 9, 2005): 411–18. http://dx.doi.org/10.1017/s0031182005009042.
Full textAbstract:
Infective larvae of an intestinal nematode,Strongyloides venezuelensis, enter rodent hosts percutaneously, and migrate through connective tissues and lungs. Then they arrive at the small intestine, where they reach maturity. It is not known howS. venezuelensislarvae develop during tissue migration. Here we demonstrate that tissue invasion ability ofS. venezuelensislarvae changes drastically during tissue migration, and that the changes are associated with stage-specific protein expression. Infective larvae, connective tissue larvae, lung larvae, and mucosal larvae were used to infect mice by various infection methods, including percutaneous, subcutaneous, oral, and intraduodenal inoculation. Among different migration stages, only infective larvae penetrated mouse skin. Larvae, once inside the host, quickly lost skin penetration ability, which was associated with the disappearance of an infective larva-specific metalloprotease. Migrating larvae had connective tissue migration ability until in the lungs, where larvae became able to settle down in the intestinal mucosa. Lung larvae and mucosal larvae were capable of producing and secreting adhesion molecules.
4
Leonard, Jill BK, and Stephen D. McCormick. "Effects of migration distance on whole-body and tissue-specific energy use in American shad (Alosa sapidissima)." Canadian Journal of Fisheries and Aquatic Sciences 56, no. 7 (July 1, 1999): 1159–71. http://dx.doi.org/10.1139/f99-041.
Full textAbstract:
We examined total and tissue-specific energy content of upstream-migrating American shad (Alosa sapidissima) in the Connecticut River. Total energy depletion over the course of the 228-km migration ranged from 35 to 60%. The approximate contributions of different tissues to energy use during migration were white muscle 57%, subdermal fat 27%, red muscle 8%, viscera 6%, and liver 2%. American shad preferentially use energy stores in the skin and its subdermal fat layer (depleted by 63%) while sparing red muscle protein. Both lipid and protein were used as energy sources throughout migration, although lipids were depleted to a greater extent (e.g., white muscle lipid decreased 48% and protein 30%). Large fish expended 2-21% more energy during migration than small fish. Migrating to upriver sites (198-228 km) is 50-100% more energetically expensive than to lower river sections for females. This suggests that upriver range expansion may be limited by females in that they may have reached a threshold level of energy expenditure in this upriver area. American shad may possess physiological mechanisms for tissue-specific energy use allowing maintenance of critical tissues necessary for postspawning survival.
5
Greer, A., K. Irie, A. Hashim, B. G. Leroux, A. M. Chang, M. A. Curtis, and R. P. Darveau. "Site-Specific Neutrophil Migration and CXCL2 Expression in Periodontal Tissue." Journal of Dental Research 95, no. 8 (March 24, 2016): 946–52. http://dx.doi.org/10.1177/0022034516641036.
Full text
6
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.
Full textAbstract:
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.
7
Mackay, Charles R., Wendy L. Marston, Lisbeth Dudler, Olivier Spertini, Thomas F. Tedder, and Wayne R. Hein. "Tissue-specific migration pathways by phenotypically distinct subpopulations of memory T cells." European Journal of Immunology 22, no. 4 (April 1992): 887–95. http://dx.doi.org/10.1002/eji.1830220402.
Full text
8
Tilmann, C., and B. Capel. "Mesonephric cell migration induces testis cord formation and Sertoli cell differentiation in the mammalian gonad." Development 126, no. 13 (July 1, 1999): 2883–90. http://dx.doi.org/10.1242/dev.126.13.2883.
Full textAbstract:
In mammals a single gene on the Y chromosome, Sry, controls testis formation. One of the earliest effects of Sry expression is the induction of somatic cell migration from the mesonephros into the XY gonad. Here we show that mesonephric cells are required for cord formation and male-specific gene expression in XY gonads in a stage-specific manner. Culturing XX gonads with an XY gonad at their surface, as a ‘sandwich’, resulted in cell migration into the XX tissue. Analysis of sandwich gonads revealed that in the presence of migrating cells, XX gonads organized cord structures and acquired male-specific gene expression patterns. From these results, we conclude that mesonephric cell migration plays a critical role in the formation of testis cords and the differentiation of XY versus XX cell types.
9
Meeusen, Els N. T., Robert R. Premier, and Mai R. Brandon. "Tissue-specific migration of lymphocytes: a key role for Th1 and Th2 cells ?" Immunology Today 17, no. 9 (September 1996): 421–24. http://dx.doi.org/10.1016/0167-5699(96)10055-4.
Full text
10
Yoon, Sungjun, and Rudolf E. Leube. "Keratin intermediate filaments: intermediaries of epithelial cell migration." Essays in Biochemistry 63, no. 5 (October 2019): 521–33. http://dx.doi.org/10.1042/ebc20190017.
Full textAbstract:
Abstract Migration of epithelial cells is fundamental to multiple developmental processes, epithelial tissue morphogenesis and maintenance, wound healing and metastasis. While migrating epithelial cells utilize the basic acto-myosin based machinery as do other non-epithelial cells, they are distinguished by their copious keratin intermediate filament (KF) cytoskeleton, which comprises differentially expressed members of two large multigene families and presents highly complex patterns of post-translational modification. We will discuss how the unique mechanophysical and biochemical properties conferred by the different keratin isotypes and their modifications serve as finely tunable modulators of epithelial cell migration. We will furthermore argue that KFs together with their associated desmosomal cell–cell junctions and hemidesmosomal cell–extracellular matrix (ECM) adhesions serve as important counterbalances to the contractile acto-myosin apparatus either allowing and optimizing directed cell migration or preventing it. The differential keratin expression in leaders and followers of collectively migrating epithelial cell sheets provides a compelling example of isotype-specific keratin functions. Taken together, we conclude that the expression levels and specific combination of keratins impinge on cell migration by conferring biomechanical properties on any given epithelial cell affecting cytoplasmic viscoelasticity and adhesion to neighboring cells and the ECM.
11
Hariharan, Nisha, Keith A. Ashcraft, Robert S. Svatek, Carolina B. Livi, Desiree Wilson, Dharam Kaushik, Robin J. Leach, and Teresa L. Johnson-Pais. "Adipose Tissue-Secreted Factors Alter Bladder Cancer Cell Migration." Journal of Obesity 2018 (2018): 1–10. http://dx.doi.org/10.1155/2018/9247864.
Full textAbstract:
Background. Obesity is associated with an increased risk of bladder cancer recurrence. This study investigated the role of adipose tissue in bladder cancer progression. Methods. Gene expression profiling was performed on adipose tissues collected from normal weight (n=5), overweight (n=11), and obese (n=10) patients with invasive bladder cancer, and adipose stromal cells (ASCs) were obtained from two normal weight, two overweight, and two obese patients. Conditioned media (CM) was characterized and evaluated for its effects on the proliferation, migration, and invasive potential of T24 bladder cancer cells. Results. Expression profiling demonstrated depot-specific or body mass index-specific differences. Increased T24 cell migration was observed using CM harvested from all ASCs. ASC CM from an obese patient significantly increased T24 cell migration and invasion compared to ASC CM collected from normal weight and overweight patients. We identified abundant expression of CXCL1, PAI1, IL6, CX3CL1, and CCL2 in all CM. Exogenous treatment of T24 cells with PAI1, IL6, and CXCL1 enhanced migration. Depletion of CXCL1, PAI1, and IL6 in an obese patient ASC CM abrogated T24 migration. Conclusion. Factors secreted by adipose tissue influence the migration of bladder tumor cells and could play an active role in tumor progression.
12
Vérollet, Christel, Shanti Souriant, Emilie Bonnaud, Paul Jolicoeur, Brigitte Raynaud-Messina, Cassandre Kinnaer, Isabelle Fourquaux, et al. "HIV-1 reprograms the migration of macrophages." Blood 125, no. 10 (March 5, 2015): 1611–22. http://dx.doi.org/10.1182/blood-2014-08-596775.
Full textAbstract:
Key PointsHIV-1 Nef reprograms human macrophage migration favoring the mesenchymal mode, which translates in vivo to macrophage tissue accumulation. Nef enhances mesenchymal migration by influencing podosome organization and function via the phagocyte-specific kinase Hck and WASP.
13
Trebaul, A., E. K. Chan, and K. S. Midwood. "Regulation of fibroblast migration by tenascin-C." Biochemical Society Transactions 35, no. 4 (July 20, 2007): 695–97. http://dx.doi.org/10.1042/bst0350695.
Full textAbstract:
Synthesis of new tissue by fibroblasts is required for tissue rebuilding in response to injury. Fibroblast migration from surrounding healthy tissue into the fibrin–fibronectin provisional matrix deposited upon injury is a key rate-limiting step of this stage of tissue repair. These events must be tightly regulated. Excessive deposition of scar tissue is the major hallmark of fibrotic disease. Tenascin-C is an extracellular matrix glycoprotein that is transiently expressed upon tissue injury, where it is specifically localized to the wound edge, and persistently up-regulated in fibrotic disease. We have shown that full-length tenascin-C promotes fibroblast migration within fibrin–fibronectin matrices and we have mapped the domains within the molecule critical for enhancing migration. We also demonstrated that specific fragments of tenascin-C inhibit fibroblast migration. These results suggest that transient expression of tenascin-C at the wound boundary is key to tissue repair: its induction recruits fibroblasts into the wound and fragments resulting from its breakdown prevent excessive fibroblast infiltration. Our results demonstrate how fibroblast migration in three-dimensional provisional matrices may be differentially regulated by proteolysis of matrix molecules and could explain how persistent expression of tenascin-C contributes to the progression of fibrotic disease.
14
Tkachev, Victor, Scott N. Furlan, E. Lake Potter, Hengqi Zheng, Daniel J. Hunt, Lucrezia Colonna, Agne Taraseviciute, et al. "Uncovering the Molecular Signature of Pathogenic Tissue-Infiltrating T Cells during Acute Graft-Versus-Host Disease." Blood 132, Supplement 1 (November 29, 2018): 805. http://dx.doi.org/10.1182/blood-2018-99-113652.
Full textAbstract:
Abstract One of the major barriers to developing targeted therapies for aGVHD control is the difficulty in identifying T cell signatures specific for GVHD pathology while distinguishing these from the pathways essential for tissue-specific T cell immune reconstitution. To address this need we have interrogated the migration patterns, as well as the phenotypic and transcriptomic characteristics of allogeneic T cells infiltrating aGVHD target organs in non-human primates. To rigorously study T cell migration during aGVHD we tracked T cells labeled following in vivo infusion with fluorescently tagged anti-CD45 antibodies given to NHP transplant recipients with aGVHD on day 8 post-HCT, during active disease. Anti-CD45 antibodies with distinct fluorescent tags were given at 6 hours before necropsy (anti-CD45-AlexaFluor647) and 5 minutes before necropsy (anti-CD45-AlexaFluor488), in order to measure T cells that were in the circulation and those migrating to GVHD target tissues, based on their labeling with one or both fluorescently-tagged antibodies. These experiments identified increased migration of both allogeneic CD8 T cells (Figure 1A) and CD4 T cells (not shown) during aGVHD, with trafficking into secondary lymphoid organs as well as non-lymphoid GVHD target organs (intestine and kidney). While migration was increased during aGVHD, these T cells, which demonstrated some phenotypic similarities to CD8 T cells in the peripheral blood (Figure 1B), also adopted tissue-specific phenotypes as measured by flow cytometry (Figure 1C), including the expression of canonical markers of resident-memory T cells (CD69+CD103-/+). However, unlike the tissue-resident T cells in healthy controls during homeostasis, tissue-infiltrating T cells during aGVHD expressed multiple markers of activation, including Ki67 and Granzyme B (Figure 1D). These flow cytometric characteristics suggested that the phenotype of organ-infiltrating T cells during aGVHD included attributes of both tissue-residency and of pathogenic alloreactivity. To further identify aGVHD-specific signatures, we performed transcriptomic analysis of tissue-infiltrating T cells during aGVHD. Using an unsupervised weighted gene correlation network analysis (WGCNA) we characterized the gene sets associated with individual GVHD target organs (Figure 2). We found that tissue-infiltrating T cells during aGVHD could be characterized by divergent features: First, they maintained a core tissue localization signature, which included genes previously linked to tissue-resident T cells (e.g. RUNX3, IFNG, CXCR6). Importantly, however, they also acquired an aGVHD-specific transcriptional signature including expression of IL1RL1 (encoding ST2), ICOS, TNFRSF9 (CD137) and TNFRSF4 (OX40). This signature also included enrichment for transcripts encoding the cytotoxic mediators GRMB and GRMA, the proliferation markers MKI67 and AURKA, as well as cytokines and cytokine receptors (IL18, IL18R, IL21, IL21R). Proteins encoded by each of these transcripts have been linked to aGVHD-causing T cells, strengthening the inference that these constitute a robust transcriptomic signature of aGVHD pathogenesis. Thus, for the first time in a large-animal model, we have been able to directly measure both the kinetics and the protein and RNA expression signatures of T cells during their migration into aGVHD target organs, This study provides new evidence for the evolution of a phenotypic and transcriptomic dichotomy during aGVHD-mediated tissue infiltration, in which T cells take on both tissue- and aGVHD-specific characteristics. These data provide novel insights into the spatial organization of systemic alloimmunity during aGVHD, which should enable more precise targeting of pathogenic T cell populations while preserving normal tissue immune reconstitution after transplantation. Disclosures Tkachev: Regeneron Pharmaceuticals, Inc.: Research Funding. Blazar:Kadmon Corporation, LLC: Consultancy, Research Funding. Kean:Regeneron Pharmaceuticals, Inc.: Research Funding.
15
Bhaumik, Vaishali, and Krushnamegh Kunte. "Dispersal and migration have contrasting effects on butterfly flight morphology and reproduction." Biology Letters 16, no. 8 (August 2020): 20200393. http://dx.doi.org/10.1098/rsbl.2020.0393.
Full textAbstract:
Movement may fundamentally alter morphology and reproductive states in insects. In long-distance migrants, reproductive diapause is associated with trade-offs between diverse life-history traits such as flight morphology and lifespan. However, many non-diapausing insects engage in shorter resource-driven dispersals. How diapause and other reproductive states alter flight morphology in migrating versus dispersing insects is poorly understood. To find out, we compared flight morphology in different reproductive states of multiple butterfly species. We found that dispersers consisted of ovulating females with higher egg loads compared with non-dispersing females. This trend was in stark contrast with that of migrating female butterflies in reproductive diapause, which made substantially higher investment in flight tissue compared with reproductively active, non-migrating females. Thus, long-distance migration and shorter resource-driven dispersals had contrasting effects on flight morphology and egg loads. By contrast, male flight morphology was not affected by dispersal, migration or associated reproductive states. Thus, dispersal and migration affected resource allocation in flight and reproductive tissue in a sex-specific manner across relatively mobile versus non-dispersing individuals of different species. These findings suggest that dispersals between fragmented habitats may put extra stress on egg-carrying females by increasing their flight burdens.
16
Chen, Chun, Bradford A. Young, Catherine S. Coleman, Anthony E. Pegg, and Dean Sheppard. "Spermidine/spermine N1-acetyltransferase specifically binds to the integrin α9 subunit cytoplasmic domain and enhances cell migration." Journal of Cell Biology 167, no. 1 (October 11, 2004): 161–70. http://dx.doi.org/10.1083/jcb.200312166.
Full textAbstract:
The integrin α9β1 is expressed on migrating cells, such as leukocytes, and binds to multiple ligands that are present at sites of tissue injury and inflammation. α9β1, like the structurally related integrin α4β1, mediates accelerated cell migration, an effect that depends on the α9 cytoplasmic domain. α4β1 enhances migration through reversible binding to the adapter protein, paxillin, but α9β1-dependent migration is paxillin independent. Using yeast two-hybrid screening, we identified the polyamine catabolizing enzyme spermidine/spermine N1-acetyltransferase (SSAT) as a specific binding partner of the α9 cytoplasmic domain. Overexpression of SSAT increased α9β1-mediated migration, and small interfering RNA knockdown of SSAT inhibited this migration without affecting cell adhesion or migration that was mediated by other integrin cytoplasmic domains. The enzyme activity of SSAT is critical for this effect, because a catalytically inactive version did not enhance migration. We conclude that SSAT directly binds to the α9 cytoplasmic domain and mediates α9-dependent enhancement of cell migration, presumably by localized effects on acetylation of polyamines or of unidentified substrates.
17
Skuratovskaia, Daria, Maria Vulf, Olga Khaziakhmatova, Vladimir Malashchenko, Aleksandra Komar, Egor Shunkin, Valeriya Shupletsova, Andrei Goncharov, Olga Urazova, and Larisa Litvinova. "Tissue-Specific Role of Macrophages in Noninfectious Inflammatory Disorders." Biomedicines 8, no. 10 (October 9, 2020): 400. http://dx.doi.org/10.3390/biomedicines8100400.
Full textAbstract:
Chronic inflammation may not begin with local tissue disorders, such as hypoxia, but with the accumulation of critically activated macrophages in one site. The purpose of this review is to analyze the data reported in the scientific literature on the features of the functions of macrophages and their contributions to the development of pathology in various tissues during aseptic inflammation in obese subjects. In individuals with obesity, increased migration of monocytes from the peripheral blood to various tissues, the proliferation of resident macrophages and a change in the balance between alternatively activated anti-inflammatory macrophages (M2) and pro-inflammatory classically activated macrophages (M1) towards the latter have been observed. The primary cause of some metabolic pathologies has been precisely identified as the recruitment of macrophages with an altered phenotype, which is probably typical for many other pathologies. Recent studies have identified phenotypes, such as metabolically activated M (MMe), oxidized (Mox), hemoglobin-related macrophages (Mhem and MHb), M4 and neuroimmunological macrophages (NAM, SAM), which directly and indirectly affect energy metabolism. The high heterogeneity of macrophages in tissues contributes to the involvement of these cells in the development of a wide range of immune responses, including pathological ones. The replenishment of tissue-specific macrophages occurs at the expense of infiltrating monocyte-derived macrophages (MoMFs) in the pathological process. The origin of MoMFs from a general precursor retains their common regulatory mechanisms and similar sensitivity to regulatory stimuli. This makes it possible to find universal approaches to the effect on these cells and, as a consequence, universal approaches for the treatment of various pathological conditions.
18
Creusot, Rémi J., Shahriar S. Yaghoubi, Pearl Chang, Justine Chia, Christopher H. Contag, Sanjiv S. Gambhir, and C. Garrison Fathman. "Lymphoid tissue–specific homing of bone marrow–derived dendritic cells." Blood 113, no. 26 (June 25, 2009): 6638–47. http://dx.doi.org/10.1182/blood-2009-02-204321.
Full textAbstract:
Abstract Because of their potent immunoregulatory capacity, dendritic cells (DCs) have been exploited as therapeutic tools to boost immune responses against tumors or pathogens, or dampen autoimmune or allergic responses. Murine bone marrow–derived DCs (BM-DCs) are the closest known equivalent of the blood monocyte-derived DCs that have been used for human therapy. Current imaging methods have proven unable to properly address the migration of injected DCs to small and deep tissues in mice and humans. This study presents the first extensive analysis of BM-DC homing to lymph nodes (and other selected tissues) after intravenous and intraperitoneal inoculation. After intravenous delivery, DCs accumulated in the spleen, and preferentially in the pancreatic and lung-draining lymph nodes. In contrast, DCs injected intraperitoneally were found predominantly in peritoneal lymph nodes (pancreatic in particular), and in omentum-associated lymphoid tissue. This uneven distribution of BM-DCs, independent of the mouse strain and also observed within pancreatic lymph nodes, resulted in the uneven induction of immune response in different lymphoid tissues. These data have important implications for the design of systemic cellular therapy with DCs, and in particular underlie a previously unsuspected potential for specific treatment of diseases such as autoimmune diabetes and pancreatic cancer.
19
David, R., and F. M. Marelli-Berg. "Regulation of T-cell migration by co-stimulatory molecules." Biochemical Society Transactions 35, no. 5 (October 25, 2007): 1114–18. http://dx.doi.org/10.1042/bst0351114.
Full textAbstract:
Migration of primed T-cells to the antigenic site is an essential event in the development of effective immunity. This process is tightly regulated in order to ensure efficient and specific responses. Most studies have focused on non-specific mediators of T-cell migration, including integrins and chemokines. However, recent studies have highlighted the key role of the T-cell receptor and co-stimulatory molecules in guiding T-cell access to antigenic tissue. Here, we review the experimental evidence for an essential contribution of co-stimulation-mediated molecular interactions regulating T-cell migration in the development of T-cell immunity and tolerance.
20
Dorfleutner, Andrea, Edith Hintermann, Takehiko Tarui, Yoshikazu Takada, and Wolfram Ruf. "Cross-talk of Integrin α3β1 and Tissue Factor in Cell Migration." Molecular Biology of the Cell 15, no. 10 (October 2004): 4416–25. http://dx.doi.org/10.1091/mbc.e03-09-0640.
Full textAbstract:
In cancer and angiogenesis, coagulation-independent roles of tissue factor (TF) in cell migration are incompletely understood. Immobilized anti-TF extracellular domain antibodies induce cell spreading, but this phenomenon is epitope specific and is not induced by anti-TF 5G9. Spreading on anti-TF is β1 integrin–dependent, indicating functional interactions of the TF extracellular domain 5G9 epitope (a presumed integrin-binding site) and integrins. Recombinant TF extracellular domain supports adhesion of cells expressing αvβ3 or certain β1 integrin heterodimers (α3β1, α4β1, α5β1, α6β1, α9β1) and adhesion is blocked by specific anti-integrin antibodies or mutations in the integrin ligand-binding site. Although several studies have linked TF to cell migration, we here demonstrate that TF specifically regulates α3β1-dependent migration on laminin 5. Expression of TF suppresses α3β1-dependent migration, but only when the TF cytoplasmic domain is not phosphorylated. Suppression of migration can be reversed by 5G9, presumably by disrupting integrin interaction, or by the protease ligand VIIa, known to induce PAR-2–dependent phosphorylation of TF. In both cases, release of α3β1 inhibition is prevented by mutation of critical phosphorylation sites in the TF cytoplasmic domain. Thus, TF influences integrin-mediated migration through cooperative intra- and extracellular interactions and phosphorylation regulates TF's function in cell motility.
21
Funderburg, F. M., and R. R. Markwald. "Conditioning of native substrates by chondroitin sulfate proteoglycans during cardiac mesenchymal cell migration." Journal of Cell Biology 103, no. 6 (December 1, 1986): 2475–87. http://dx.doi.org/10.1083/jcb.103.6.2475.
Full textAbstract:
It is generally proposed that embryonic mesenchymal cells use sulfated macromolecules during in situ migration. Attempts to resolve the molecular mechanisms for this hypothesis using planar substrates have been met with limited success. In the present study, we provide evidence that the functional significance of certain sulfated macromolecules during mesenchyme migration required the presence of the endogenous migratory template; i.e., native collagen fibrils. Using three-dimensional collagen gel lattices and whole embryo culture procedures to produce metabolically labeled sulfated macromolecules in embryonic chick cardiac tissue, we show that these molecules were primarily proteoglycan (PG) in nature and that their distribution was class specific; i.e., heparan sulfate PG, the minor labeled component (15%), remained pericellular while chondroitin sulfate (CS) PG, the predominately labeled PG (85%), was associated with collagen fibrils as "trails" of 50-60-nm particles when viewed by scanning electron microscopy. Progressive "conditioning" of collagen with CS-PG inhibited the capacity of the template to support subsequent cell migration. Lastly, metabolically labeled, PG-derived CS chains were compared with respect to degree of sulfation in either the C-6 or C-4 position by chromatographic separation of chondroitinase AC digestion products. Results from temporal and regional comparisons of in situ-labeled PGs indicated a positive correlation between the presence of mesenchyme and an enrichment of disaccharide-4S relative to that from regions lacking mesenchyme (i.e., principally myocardial tissue). The suggestion of a mesenchyme-specific CS-PG was substantiated by similarly examining the PGs synthesized solely by cardiac mesenchymal cells migrating within hydrated collagen lattice in culture. These data were incorporated into a model of "substratum conditioning" which provides a molecular mechanism by which secretion of mesenchyme-specific CS-PGs not only provides for directed and sustained cell movement, but ultimately inhibits migration of the cell population as a whole.
22
Starr, Daniel A., Greg J. Hermann, Christian J. Malone, William Fixsen, James R. Priess, H. Robert Horvitz, and Min Han. "unc-83encodes a novel component of the nuclear envelope and is essential for proper nuclear migration." Development 128, no. 24 (December 15, 2001): 5039–50. http://dx.doi.org/10.1242/dev.128.24.5039.
Full textAbstract:
Nuclear migration plays an essential role in the growth and development of a wide variety of eukaryotes. Mutations in unc-84, which encodes a conserved component of the nuclear envelope, have been shown to disrupt nuclear migration in two C. elegans tissues. We show that mutations in unc-83 disrupt nuclear migration in a similar manner in migrating P cells, hyp7 precursors and the intestinal primordium, but have no obvious defects in the association of centrosomes with nuclei or the structure of the nuclear lamina of migrating nuclei. We also show that unc-83 encodes a novel transmembrane protein. We identified three unc-83 transcripts that are expressed in a tissue-specific manner. Antibodies against UNC-83 co-localized to the nuclear envelope with lamin and UNC-84. Unlike UNC-84, UNC-83 localized to only specific nuclei, many of which were migratory. UNC-83 failed to localize to the nuclear envelope in unc-84 mutants with lesions in the conserved SUN domain of UNC-84, and UNC-83 interacted with the SUN domain of UNC-84 in vitro, suggesting that these two proteins function together during nuclear migration. We favor a model in which UNC-84 directly recruits UNC-83 to the nuclear envelope where they help transfer force between the cytoskeleton and the nucleus.
23
Desando, Giovanna, Isabella Bartolotti, Lucia Martini, Gianluca Giavaresi, Nicolò Nicoli Aldini, Milena Fini, Alice Roffi, et al. "Regenerative Features of Adipose Tissue for Osteoarthritis Treatment in a Rabbit Model: Enzymatic Digestion Versus Mechanical Disruption." International Journal of Molecular Sciences 20, no. 11 (May 29, 2019): 2636. http://dx.doi.org/10.3390/ijms20112636.
Full textAbstract:
Evaluating cell migration after cell-based treatment is important for several disorders, including osteoarthritis (OA), as it might influence the clinical outcome. This research explores migrating expanded-adipose stromal cells (ASCs) and adipose niches after enzymatic and mechanical processes. Bilateral anterior cruciate ligament transection induced a mild grade of OA at eight weeks in adult male New Zealand rabbits. ASCs, enzymatic stromal vascular fraction (SVF), and micro fragmented adipose tissue (MFAT) were intra-articularly injected in the knee joint. Assessments of cell viability and expression of specific markers, including CD-163 wound-healing macrophages, were done. Cell migration was explored through labelling with PKH26 dye at 7 and 30 days alongside co-localization analyses for CD-146. All cells showed good viability and high percentages of CD-90 and CD-146. CD-163 was significantly higher in MFAT compared to SVF. Distinct migratory potential and time-dependent effects were observed among cell-based treatments. At day 7, both ASCs and SVF migrated towards synovium, whereas for MFAT versus cartilage, a different migration pattern was noticed at day 30. The long-term distinct cell migration of ASCs, SVF, and MFAT open interesting clinical insights on their potential use for OA treatment. Moreover, the highest expression of CD-163 in MFAT, rather than SVF, might have an important role in directly mediating cartilage tissue repair responses.
24
Marelli-Berg, Federica M., Martha J. James, John Dangerfield, Julian Dyson, Maggie Millrain, Diane Scott, Elizabeth Simpson, Sussan Nourshargh, and Robert I. Lechler. "Cognate recognition of the endothelium induces HY-specific CD8+ T-lymphocyte transendothelial migration (diapedesis) in vivo." Blood 103, no. 8 (April 15, 2004): 3111–16. http://dx.doi.org/10.1182/blood-2003-08-2717.
Full textAbstract:
Abstract The physiologic significance of MHC-peptide complex presentation by endothelial cells (ECs) to trafficking T lymphocytes remains unresolved. On the basis of our observation that cognate recognition of ECs enhanced transendothelial migration of antigen-specific T lymphocytes in vitro, we have proposed that by displaying antigenic peptides from the underlying tissue, ECs promote the recruitment of antigen-specific T cells. In this study, we have tested this hypothesis by comparing the trafficking of HY-specific T lymphocytes into antigenic and nonantigenic tissue using in vivo models of T-cell recruitment. Up-regulated expression of H2 molecules presenting endogenous antigen in the peritoneal mesothelium and vessels led to the local recruitment of HY-specific T cells in male, but not female, mice. Intravital microscopy experiments analyzing EC–HY-specific T-cell interactions in the cremasteric vascular bed revealed that cognate recognition of the endothelium results in enhanced diapedesis of T cells into the tissue, while not affecting rolling and adhesion. Our results are consistent with the hypothesis that, under inflammatory conditions, antigen presentation by the endothelium contributes to the development and specificity of T-cell–mediated inflammation by favoring the selective migration of antigen-specific T cells. (Blood. 2004;103:3111-3116)
25
Tauzin, Sebastien, Taylor W. Starnes, Francisco Barros Becker, Pui-ying Lam, and Anna Huttenlocher. "Redox and Src family kinase signaling control leukocyte wound attraction and neutrophil reverse migration." Journal of Cell Biology 207, no. 5 (December 8, 2014): 589–98. http://dx.doi.org/10.1083/jcb.201408090.
Full textAbstract:
Tissue damage induces early recruitment of neutrophils through redox-regulated Src family kinase (SFK) signaling in neutrophils. Redox-SFK signaling in epithelium is also necessary for wound resolution and tissue regeneration. How neutrophil-mediated inflammation resolves remains unclear. In this paper, we studied the interactions between macrophages and neutrophils in response to tissue damage in zebrafish and found that macrophages contact neutrophils and induce resolution via neutrophil reverse migration. We found that redox-SFK signaling through p22phox and Yes-related kinase is necessary for macrophage wound attraction and the subsequent reverse migration of neutrophils. Importantly, macrophage-specific reconstitution of p22phox revealed that macrophage redox signaling is necessary for neutrophil reverse migration. Thus, redox-SFK signaling in adjacent tissues is essential for coordinated leukocyte wound attraction and repulsion through pathways that involve contact-mediated guidance.
26
Mirenda, Vincenzo, Sarah J. Jarmin, Rachel David, Julian Dyson, Diane Scott, Yan Gu, Robert I. Lechler, Klaus Okkenhaug, and Federica M. Marelli-Berg. "Physiologic and aberrant regulation of memory T-cell trafficking by the costimulatory molecule CD28." Blood 109, no. 7 (November 21, 2006): 2968–77. http://dx.doi.org/10.1182/blood-2006-10-050724.
Full textAbstract:
Abstract Productive T-cell immunity requires both the activation and the migration of specific T cells to the antigenic tissue. The costimulatory molecule CD28 plays an essential role in the initiation of T-cell–mediated immunity. We investigated the possibility that CD28 may also regulate migration of primed T cells to target tissue. In vitro, CD28-mediated signals enhanced T-cell transendothelial migration, integrin clustering, and integrin-mediated migration. In vivo, T cells bearing a mutation in the CD28 cytoplasmic domain, which abrogates PI3K activation, displayed normal clonal expansion but defective localization to antigenic sites following antigenic rechallenge. Importantly, antibody-mediated CD28 stimulation led to unregulated memory T-cell migration to extra-lymphoid tissue, which occurred independently of T-cell receptor (TCR)–derived signals and homing-receptor expression. Finally, we provide evidence that CD28- and CTLA-4–mediated signals exert opposite effects on T-cell trafficking in vivo. These findings highlight a novel physiologic function of CD28 that has crucial implications for the therapeutic manipulation of this and other costimulatory molecules.
27
Veličković, Nataša, Ana Djordjevic, Ana Vasiljević, Biljana Bursać, Danijela Vojnović Milutinović, and Gordana Matić. "Tissue-specific regulation of inflammation by macrophage migration inhibitory factor and glucocorticoids in fructose-fed Wistar rats." British Journal of Nutrition 110, no. 3 (January 3, 2013): 456–65. http://dx.doi.org/10.1017/s0007114512005193.
Full textAbstract:
High fructose consumption is commonly associated with insulin resistance, disturbed glucose homeostasis and low-grade inflammation. Increased glucocorticoid production within adipose tissue has been implicated in the pathogenesis of fructose-induced metabolic syndrome. Immunosuppressive actions of glucocorticoids can be counter-regulated by macrophage migration inhibitory factor (MIF), which is recognised as a key molecule in metabolic inflammation. In the present study, we hypothesised that coordinated action of glucocorticoids and MIF can mediate the effects of a high-fructose diet on adipose tissue and liver inflammation. We examined the effects of long-term consumption of a 10 % fructose solution on corticosterone (CORT) and MIF levels in rat blood plasma, liver and adipose tissue, as well as MIF and TNF-α mRNA expression and NF-κB activation in the same tissues. The high-fructose diet led to an increase in both CORT and MIF in the adipose tissue, and a highly significant positive correlation between their levels was observed. The attenuated NF-κB activation and unaltered TNF-α mRNA expression noticed in the adipose tissue could be interpreted as an outcome of the opposing actions of CORT and MIF. In contrast to adipose tissue, inflammation in the liver was characterised by NF-κB activation, an increased TNF-α mRNA level and unchanged levels of MIF protein, MIF mRNA and CORT. Overall, these findings suggest that a high-fructose diet differently affects the levels of glucocorticoids and MIF in the adipose tissue and liver, implicating that fructose over-consumption has tissue-specific effects on regulation of metabolic inflammation.
28
Lefranc, Florence, Jacques Brotchi, and Robert Kiss. "Possible Future Issues in the Treatment of Glioblastomas: Special Emphasis on Cell Migration and the Resistance of Migrating Glioblastoma Cells to Apoptosis." Journal of Clinical Oncology 23, no. 10 (April 1, 2005): 2411–22. http://dx.doi.org/10.1200/jco.2005.03.089.
Full textAbstract:
Purpose The present review aims to emphasize that malignant gliomas are characterized by the diffuse invasion of distant brain tissue by a myriad of single migrating cells that exhibit decreased levels of apoptosis (programmed cell death type I), thus a resistance to cytotoxic insult. Methods The present review surveys the molecular mechanisms of migration in malignant gliomas and potential issues arising from treatments, in addition to relationships between glioma cell migration and resistance to apoptosis in terms of the molecular signaling pathways. Results Clinical and experimental data demonstrate that glioma cell migration is a complex combination of multiple molecular processes, including the alteration of tumor cell adhesion to a modified extracellular matrix, the secretion of proteases by the cells, and modifications to the actin cytoskeleton. Intracellular signaling pathways involved in the acquisition of resistance to apoptosis by migrating glioma cells concern PI3K, Akt, mTOR, NF-κB, and autophagy (programmed cell death type II). Conclusion A number of signaling pathways can be constitutively activated in migrating glioma cells, thus rendering these cells resistant to cytotoxic insults. However, these pathways are not all constitutively activated at the same time in any one glioma. Particular inhibitors should therefore only be chosen if the target is present in the tumor tissue, but this is only possible if individual patients are submitted to the molecular profiling of their tumors before undergoing any treatment to combat their migratory glioma cells. Specific antimigratory compounds should be added to conventional radio- and/or chemotherapy.
29
Ou, Rong, Menghua Zhang, Lei Huang, Richard A. Flavell, Pandelakis A. Koni, and Demetrius Moskophidis. "Regulation of Immune Response and Inflammatory Reactions against Viral Infection by VCAM-1." Journal of Virology 82, no. 6 (January 23, 2008): 2952–65. http://dx.doi.org/10.1128/jvi.02191-07.
Full textAbstract:
ABSTRACT The migration of activated antigen-specific immune cells to the target tissues of virus replication is controlled by the expression of adhesion molecules on the vascular endothelium that bind to ligands on circulating lymphocytes. Here, we demonstrate that the adhesion pathway mediated by vascular cell adhesion molecule 1 (VCAM-1) plays a role in regulating T-cell-mediated inflammation and pathology in nonlymphoid tissues, including the central nervous system (CNS) during viral infection. The ablation of VCAM-1 expression from endothelial and hematopoietic cells using a loxP-Cre recombination strategy had no major effect on the induction or overall tissue distribution of antigen-specific T cells during a systemic infection with lymphocytic choriomeningitis virus (LCMV), except in the case of lung tissue. However, enhanced resistance to lethal LCM and the significantly reduced magnitude and duration of footpad swelling observed in VCAM-1 mutant mice compared to B6 controls suggest a significant role for VCAM-1 in promoting successful local inflammatory reactions associated with efficient viral clearance and even life-threatening immunopathology under particular infection conditions. Interestingly, analysis of the infiltrating populations in the brains of intracerebrally infected mice revealed that VCAM-1 deletion significantly delayed migration into the CNS of antigen-presenting cells (macrophages and dendritic cells), which are critical for optimal stimulation of migrating virus-specific CD8+ T cells initiating a pathological cascade. We propose that the impaired migration of these accessory cells in the brain may explain the improved clinical outcome of infection in VCAM-1 mutant mice. Thus, these results underscore the potential role of VCAM-1 in regulating the immune response and inflammatory reactions against viral infections.
30
Chieosilapatham, Panjit, Shigaku Ikeda, Hideoki Ogawa, and Francois Niyonsaba. "Tissue-specific Regulation of Innate Immune Responses by Human Cathelicidin LL-37." Current Pharmaceutical Design 24, no. 10 (May 28, 2018): 1079–91. http://dx.doi.org/10.2174/1381612824666180327113418.
Full textAbstract:
Cathelicidins form one of the major families of antimicrobial peptides and have been identified in many vertebrates, including humans. LL-37, the only human member of the cathelicidin family, is detected in most sites of the human body that is normally exposed to microbes, including the epithelial lining of the skin, gastrointestinal tract, genitourinary tract and lungs. This peptide is also expressed by a variety of epithelial cells and immune cells, such as neutrophils, monocytes and mast cells. LL-37 has emerged as a key component of innate immunity due to its direct antimicrobial activity against a broad spectrum of invading pathogens. It also exhibits diverse immunomodulatory functions by activating both pro- and anti-inflammatory mediators; inducing cell migration, proliferation and differentiation; and regulating apoptosis of epithelial cells and neutrophils. Given that the phenotypic and functional properties of immune compartments are different and significantly impacted by the anatomical sites, tissue-specific factors of host origin and microbial communities play important roles in the regulation of LL-37. This review summarizes the expression and biological functions of LL-37 and discusses its significant roles in the innate immune system based on its anatomical distribution.
31
Takeuchi, Yuichiro, Keishi Yamauchi, Junko Nakamura, Satoshi Shigematsu, and Kiyoshi Hashizume. "Angiotensin II regulates migration in mouse cultured mesangial cells: evidence for the presence of receptor subtype-specific regulation." Journal of Endocrinology 191, no. 2 (November 2006): 361–67. http://dx.doi.org/10.1677/joe.1.06860.
Full textAbstract:
The biological effects of angiotensin II (AngII) are mediated by two major subtypes of AngII receptors, type 1 (AT1R) and type 2 (AT2R). In this study, we attempted to elucidate the role of AngII subtype receptor-specific regulation in migration and proliferation of mouse cultured mesangial (MSG) cells. We found that 100 nM AngII stimulated weak migration of MSG cells. Cell motility increased more in the presence of AT2R than in the presence of AT1R, and it was suppressed by guanylate cyclase inhibitors. On the other hand, the activation of AT1R resulted in increased cell numbers, while AT2R activation inhibited cell proliferation. Moreover, high concentrations of glucose (25 mM) stimulated the expression of AT2R but not AT1R. These results indicate that there are receptor subtype-specific roles in MSG cells, and it is therefore possible that the activation of AT2R stimulates repair of glomerular tissue defect, by regulation of migration and proliferation of MSG cells. Taken together, these results suggest that the relative concentrations of AT1R and AT2R are important factors in the regulation of AngII function in glomerular tissue, and alterations in the concentrations of these receptors may contribute to progression of or protection from diabetic nephropathy.
32
David, Rachel, Liang Ma, Aleksandar Ivetic, Aya Takesono, Anne J. Ridley, Jian-Guo Chai, Victor L. Tybulewicz, and Federica M. Marelli-Berg. "T-cell receptor– and CD28-induced Vav1 activity is required for the accumulation of primed T cells into antigenic tissue." Blood 113, no. 16 (April 16, 2009): 3696–705. http://dx.doi.org/10.1182/blood-2008-09-176511.
Full textAbstract:
Abstract Localization of primed T cells to antigenic tissue is essential for the development of effective immunity. Together with tissue-selective homing molecules, T-cell receptor (TCR)– and CD28-mediated signals have been shown to promote transendothelial migration of specific T cells into nonlymphoid antigen-rich tissue. However, the cellular and molecular requirements for T-cell accumulation to target tissue following their recruitment are largely undefined. The guanine nucleotide exchange factor (GEF) Vav1 has an integral role in coupling TCR and CD28 to signaling pathways that regulate T-cell activation and migration. Here, we have investigated the contribution of TCR- and CD28-induced Vav1 activity to the trafficking and localization of primed HY-specific CD4+ T cells to antigenic sites. Severe migratory defects displayed by Vav1−/− T cells in vitro were fully compensated by a combination of shear flow and chemokines, leading to normal recruitment of Vav1−/− T cells in vivo. In contrast, Vav1−/− T-cell retention into antigen-rich tissue was severely impaired, reflecting T cells' inability to engage in sustained TCR- and CD28-mediated interactions with tissue-resident antigen-presenting cells (APCs). This novel function of APC-induced, and TCR- and CD28-mediated Vav1 activity in the regulation of effector T-cell immunity highlights its potential as a therapeutic target in T cell–mediated tissue damage.
33
McCormack, S. A., J. Y. Wang, M. J. Viar, L. Tague, P. J. Davies, and L. R. Johnson. "Polyamines influence transglutaminase activity and cell migration in two cell lines." American Journal of Physiology-Cell Physiology 267, no. 3 (September 1, 1994): C706—C714. http://dx.doi.org/10.1152/ajpcell.1994.267.3.c706.
Full textAbstract:
Transglutaminases (TGAs) catalyze the cross-linking of proteins through formation of gamma-glutaminyl-epsilon-lysine bonds and incorporation of small-molecular-weight amines, including polyamines, into the gamma-glutamine sites of proteins. Tissue TGA has been shown to establish covalent cross-links between cytoskeletal proteins using polyamines as substrates, and protein-polyamine conjugates have been identified in a variety of cells. We have shown previously that polyamines are required for cell migration in IEC-6 cells [S. A. McCormack, M. J. Viar, and L. R. Johnson. Am. J. Physiol. 264 (Gastrointest. Liver Physiol. 27): G367-G374, 1993]. In this study, we explored the relationship between cell migration, polyamines, and tissue TGA activity in two cell lines and found that while both IEC-6 and Caco-2 cells required normal levels of polyamines to migrate across a denuded surface, tissue TGA activity responded differently to polyamine deficiency brought about by treatment with alpha-difluoromethylornithine (DFMO). DFMO is a specific and irreversible inhibitor of ornithine decarboxylase, a rate-limiting enzyme of polyamine biosynthesis. In IEC-6 cells, tissue TGA activity decreased significantly with DFMO treatment concurrent with a rise in inactive TGA protein as measured by Western blot analysis. On the other hand, in Caco-2 cells, tissue TGA activity and protein increased significantly with DFMO treatment. In both cell lines, addition of polyamines to the DFMO treatment restored cell migration, tissue TGA activity, and protein to control levels.(ABSTRACT TRUNCATED AT 250 WORDS)
34
Jaglarz, M. K., and K. R. Howard. "Primordial germ cell migration in Drosophila melanogaster is controlled by somatic tissue." Development 120, no. 1 (January 1, 1994): 83–89. http://dx.doi.org/10.1242/dev.120.1.83.
Full textAbstract:
In Drosophila, as in many other organisms, primordial germ cells show invasive and migratory behavior moving from their site of origin to the somatic component of the gonad. At a characteristic time in development, the primordial germ cells pass across the primordium of the gut and migrate on its outer surface toward the mesoderm, where they eventually associate with the somatic tissues of the gonad. Here we demonstrate that the exit and migration are specific behaviors of the primordial germ cells and that they are controlled by the somatic tissue of the embryo rather than by a germ cell autonomous clock. Using mutations, we show that these controlling somatic events probably occur in the tissue of the gut primordium itself.
35
Werr, Joachim, Xun Xie, Per Hedqvist, Erkki Ruoslahti, and Lennart Lindbom. "β1 Integrins Are Critically Involved in Neutrophil Locomotion in Extravascular Tissue In Vivo." Journal of Experimental Medicine 187, no. 12 (June 15, 1998): 2091–96. http://dx.doi.org/10.1084/jem.187.12.2091.
Full textAbstract:
Recruitment of leukocytes from blood to tissue in inflammation requires the function of specific cell surface adhesion molecules. The objective of this study was to identify adhesion molecules that are involved in polymorphonuclear leukocyte (PMN) locomotion in extravascular tissue in vivo. Extravasation and interstitial tissue migration of PMNs was induced in the rat mesentery by chemotactic stimulation with platelet-activating factor (PAF; 10−7 M). Intravital time-lapse videomicroscopy was used to analyze migration velocity of the activated PMNs, and the modulatory influence on locomotion of locally administered antibodies or peptides recognizing various integrin molecules was examined. Immunofluorescence flow cytometry revealed increased expression of α4, β1, and β2 integrins on extravasated PMNs compared with blood PMNs. Median migration velocity in response to PAF stimulation was 15.5 ± 4.5 μm/min (mean ± SD). Marked reduction (67 ± 7%) in motility was observed after treatment with mAb blocking β1 integrin function (VLA integrins), whereas there was little, although significant, reduction (22 ± 13%) with β2 integrin mAb. Antibodies or integrin-binding peptides recognizing α4β1, α5β1, or αvβ3 were ineffective in modulating migration velocity. Our data demonstrate that cell surface expression of β1 integrins, although limited on blood PMNs, is induced in extravasated PMNs, and that members of the β1 integrin family other than α4β1 and α5β1 are critically involved in the chemokinetic movement of PMNs in rat extravascular tissue in vivo.
36
Krakhmal, N. V., M. V. Zavyalova, E. V. Denisov, S. V. Vtorushin, and V. M. Perelmuter. "Cancer Invasion: Patterns and Mechanisms." Acta Naturae 7, no. 2 (June 15, 2015): 17–28. http://dx.doi.org/10.32607/20758251-2015-7-2-17-28.
Full textAbstract:
Cancer invasion and the ability of malignant tumor cells for directed migration and metastasis have remained a focus of research for many years. Numerous studies have confirmed the existence of two main patterns of cancer cell invasion: collective cell migration and individual cell migration, by which tumor cells overcome barriers of the extracellular matrix and spread into surrounding tissues. Each pattern of cell migration displays specific morphological features and the biochemical/molecular genetic mechanisms underlying cell migration. Two types of migrating tumor cells, mesenchymal (fibroblast-like) and amoeboid, are observed in each pattern of cancer cell invasion. This review describes the key differences between the variants of cancer cell migration, the role of epithelial-mesenchymal, collective-amoeboid, mesenchymal-amoeboid, and amoeboid-mesenchymal transitions, as well as the significance of different tumor factors and stromal molecules in tumor invasion. The data and facts collected are essential to the understanding of how the patterns of cancer cell invasion are related to cancer progression and therapy efficacy. Convincing evidence is provided that morphological manifestations of the invasion patterns are characterized by a variety of tissue (tumor) structures. The results of our own studies are presented to show the association of breast cancer progression with intratumoral morphological heterogeneity, which most likely reflects the types of cancer cell migration and results from different activities of cell adhesion molecules in tumor cells of distinct morphological structures.
37
Orrington-Myers, Janie, Xiaopei Gao, Panos Kouklis, Michael Broman, Arshad Rahman, Stephen M. Vogel, and Asrar B. Malik. "Regulation of lung neutrophil recruitment by VE-cadherin." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 4 (October 2006): L764—L771. http://dx.doi.org/10.1152/ajplung.00502.2005.
Full textAbstract:
Lung inflammatory disease is characterized by increased polymorphonuclear leukocyte (PMN) infiltration and vascular permeability. PMN infiltration into tissue involves signaling between endothelial cells and migrating PMNs, which leads to alterations in the organization of adherens junctions (AJs). We addressed the possible role of the protein constituents of AJs, endothelium-specific vascular-endothelial (VE)-cadherin, in the migration of PMNs. Studies were made using VE-cadherin mutant constructs lacking the extracellular domain (ΔEXD) or, additionally, lacking the COOH-terminus β-catenin-binding domain (ΔEXDΔβ). Either construct was transduced in pulmonary microvessel endothelia of mice using cationic liposome-encapuslated cDNA constructs injected intravenously. Optimal expression of constructs was seen by Western blot analysis within 24 h. Vessel wall liquid permeability measured as the lung microvessel capillary filtration coefficient increased threefold in ΔEXD-transduced lungs, indicating patency of interendothelial junctions, whereas the control ΔEXDΔβ construct was ineffective. To study lung tissue PMN recruitment, we challenged mice intraperitoneally with LPS (3 mg/kg) for 6 h and measured PMN numbers by bronchoalveolar lavage and their accumulation morphometrically in lung tissue. ΔEXD expression markedly reduced the PMN sequestration and migration seen in nontransfected (control wild type) or ΔEXDΔβ-transfected (negative control) mice challenged with LPS. In addition, ΔEXD transfection suppressed LPS-induced activation of NF-κB and consequent ICAM-1 expression. These results suggest that disassembly of VE-cadherin junctions serves as a negative signal for limiting transendothelial PMN migration secondary to decreased ICAM-1 expression in the mouse model of LPS-induced sepsis.
38
Olson, Janelle A., Robert Zeiser, Andreas Beilhack, and Robert S. Negrin. "Tissue-Specific Homing of Natural Killer Cells in Allogeneic Bone Marrow Transplantation." Blood 108, no. 11 (November 16, 2006): 922. http://dx.doi.org/10.1182/blood.v108.11.922.922.
Full textAbstract:
Abstract Cell trafficking to distinct anatomical sites is critical for in vivo function. Natural Killer (NK) cells have been demonstrated to suppress graft-versus-host disease (GVHD) while inducing a graft-versus-tumor response (GVT). However, little is known about the homing of NK cells following bone marrow transplantation (BMT), their proliferative capacity and how long they persist in vivo. To investigate this, we transplanted highly purified DX5+ CD3− NK cells from FVB L2G85 luciferase+ mice into lethally irradiated syngeneic and BALB/c allogeneic recipients. Bioluminescence imaging (BLI) of transplant recipients revealed distinct NK cell migration to and proliferation in secondary lymphoid organs, which was confirmed by CFSE proliferation analysis. The allogeneic NK cells persisted for 20–30 days after which the signal gradually declined. Proliferation in lymphoid organs was undetectable in syngeneic recipients, but was enhanced by daily intraperitoneal injection of IL-2. Moderate proliferation in lymphoid organs and dramatic expansion in the thymus and peritoneal cavity were observed, which persisted for the duration of IL-2 administration. Exogenous IL-2 also increased NK cell proliferation in the allogeneic recipient thymus and peritoneal cavity, and even more robustly enhanced proliferation in the secondary lymphoid organs. Corresponding to this observed thymic homing, splenic NK cells reisolated from allogeneic recipients 5 days after transplant upregulated CCR9, a receptor important in thymocyte migration and homing of T cells to the gut. In this allogeneic setting, ex vivo imaging of the spleen and gut region 3 and 5 days after transplant confirmed localization of NK cells to the mesenteric lymph nodes, and also revealed NK cell infiltration of the small intestine, a major site of GVHD pathology in addition to the skin and liver. Additionally, donor NK cells were visible in the skin of transplanted animals by immunohistochemistry staining. Similar to T cells, a subset of freshly isolated NK cells express α4β7 and P-selectin ligand, expression of which are required for homing to the gut and skin, respectively. FACS analysis revealed that both these markers were upregulated on splenic NK cells reisolated from allogeneic recipients 5 days post-transplant. However, in contrast to T cells, CD62L was not downregulated on these NK cells. These results raised the question of whether the NK cell homing pattern observed in vivo and reflected in the upregulation of tissue-specific homing receptors is a consequence of the conditioning and transplant regime and associated inflammatory conditions, or whether NK cell alloreactivity can induce a specific trafficking pattern. To address this question, purified FVB luc+ NK cells were transplanted into unirradiated allogeneic BALB/c RAG2−/− γc −/− recipients, which lack T, B and NK cells. Moderate proliferation was seen in the spleen and lymph nodes, and infiltration of the gut tissue was observed. This implies that the inflammatory environment caused by tissue damage due to irradiation of recipients is not required for NK cell infiltration into GVHD target organs such as the gut. These studies indicate that NK cells are capable of proliferation in vivo either due to alloresponses or cytokine stimulation. Further, NK cells infiltrate GVHD target organs yet do not cause significant GVHD pathology possibly due to reduced tissue damage. NK cells may further reduce T cell proliferation in GVHD target sites through production of anti-inflammatory cytokines or by modulating antigen presentation.
39
Oksala, O., T. Salo, R. Tammi, L. Häkkinen, M. Jalkanen, P. Inki, and H. Larjava. "Expression of proteoglycans and hyaluronan during wound healing." Journal of Histochemistry & Cytochemistry 43, no. 2 (February 1995): 125–35. http://dx.doi.org/10.1177/43.2.7529785.
Full textAbstract:
We investigated the expression of proteoglycans (PGs) and hyaluronan (HA) during healing of human mucosal wounds. Biopsy specimens of experimental wounds were taken 1, 3, and 7 days after wounding. Frozen sections were used for immunolocalization of CD44, syndecan-1, basement membrane-associated heparan sulfate proteoglycan (BM-HSPG), decorin, and biglycan. HA was localized in paraffin sections with a specific HA-binding probe. Epithelium showed first signs of migration on Day 1, more progressive migration on Day 3, and epithelial sheets confronted on Day 7. CD44 surrounded migrating keratinocytes at all stages of wound healing. In epithelium, CD44 and HA remarkably localized to the same region. Expression of syndecan-1 was switched from the suprabasal cell layer of unwounded epithelium to the basal cell layer of the migrating wound epithelium. BM-HSPG was absent under migrating keratinocytes. It started to reappear at the basement membrane zone on Day 7. The area under the wound epithelium containing newly synthesized collagen fibers first became positive for decorin on Day 7, whereas staining of biglycan was negative. Granulation tissue was also strongly positive for CD44 and hyaluronan. Our results indicate that migrating keratinocytes express both CD44 and syndecan-1 but not BM-HSPG. During differentiation of keratinocytes, expression of CD44 preceded that of syndecan-1. The results suggest that different HSPGs have multiple functions in keratinocyte migration and differentiation during reepithelialization.
40
Um, Ti-Young, Seoung-Ae Lee, Joo-Hoo Park, Jae-Min Shin, Il-Ho Park, and Heung-Man Lee. "Role of Adenosine Monophosphate-Activated Protein Kinase on Cell Migration, Matrix Contraction, and Matrix Metalloproteinase-1 and Matrix Metalloproteinase-2 Production in Nasal Polyp–Derived Fibroblasts." American Journal of Rhinology & Allergy 31, no. 6 (November 2017): 357–63. http://dx.doi.org/10.2500/ajra.2017.31.4477.
Full textAbstract:
Purpose Activation of adenosine monophosphate-activated protein kinase (AMPK) by metformin, as a master regulator of metabolism, is involved in airway tissue remodeling. Here, we investigated the physical role of AMPK on cell migration, matrix contraction, and the production of matrix metalloproteinases (MMP) in nasal polyp–derived fibroblasts (NPDF). Methods Primary NPDFs from six patients with chronic rhinosinusitis and nasal polyps were isolated and cultured. To assess the effect of AMPK on fibroblast migration, we conducted scratch and migration assays in NPDF treated with metformin and/or compound C. A collagen gel contraction assay measured activity of contractile. MMP expression was measured with reverse transcription-polymerase chain reaction, Western blot, and zymography. To evaluate for specific AMPK action, we examined by AMPK small interfering RNA. Results Metformin, an activator of AMPK, significantly inhibited cell migration in NPDFs in a dose-dependent manner. Compound C, an inhibitor of AMPK, partially reversed the inhibitory effect of metformin. Metformin also significantly decreased contractile activity, with a concomitant reduction in the production of MMP-1 and MMP-2 but not of MMP-9. Specific silencing that targeted AMPK resulted in the enhancement of mobility and contractility and in the production of MMP-1 and MMP-2. Conclusion AMPK played an important role in regulating cell migration, matrix contraction, and MMP production in NPDFs, which provided data that AMPK activator might be a therapeutic target for the prevention of tissue remodeling in nasal polyps.
41
Mauduit, Olivier, Vanessa Delcroix, Tom Lesluyes, Gaëlle Pérot, Pauline Lagarde, Lydia Lartigue, Jean-Yves Blay, and Frédéric Chibon. "Recurrent DMD Deletions Highlight Specific Role of Dp71 Isoform in Soft-Tissue Sarcomas." Cancers 11, no. 7 (July 1, 2019): 922. http://dx.doi.org/10.3390/cancers11070922.
Full textAbstract:
Soft-tissue sarcomas (STS) are rare tumors whose oncogenesis remains unknown and for which no common therapeutic target has yet been identified. Analysis of 318 STS by CGH array evidenced a frequent deletion affecting the DMD gene (encoding dystrophin isoforms) in 16.5% of STS, including sarcomas with complex genomics, gastrointestinal tumors (GIST), and synovial sarcomas (SS). These deletions are significantly associated with metastatic progression, thus suggesting the role of DMD downregulation in the acquisition of aggressive phenotypes. We observed that targeted deletions of DMD were restricted to the 5’ region of the gene, which is responsible for the transcription of Dp427. Analysis of STS tumors and cell lines by RNA sequencing revealed that only the Dp71 isoform was widely expressed. Dp427 depletion had no effect on cell growth or migration. However, Dp71 inhibition by shRNA dramatically reduced the cell proliferation and clonogenicity of three STS cell lines, likely by altering the cell cycle progression through the G2/M-phase. Our work demonstrates that DMD deletions are not restricted to myogenic tumors and could be used as a biomarker for metastatic evolution in STS. Dp71 seems to play an essential role in tumor growth, thus providing a potential target for future STS treatments.
42
Shim, Gawoon, Danelle Devenport, and Daniel J. Cohen. "Overriding native cell coordination enhances external programming of collective cell migration." Proceedings of the National Academy of Sciences 118, no. 29 (July 16, 2021): e2101352118. http://dx.doi.org/10.1073/pnas.2101352118.
Full textAbstract:
As collective cell migration is essential in biological processes spanning development, healing, and cancer progression, methods to externally program cell migration are of great value. However, problems can arise if the external commands compete with strong, preexisting collective behaviors in the tissue or system. We investigate this problem by applying a potent external migratory cue—electrical stimulation and electrotaxis—to primary mouse skin monolayers where we can tune cell–cell adhesion strength to modulate endogenous collectivity. Monolayers with high cell–cell adhesion showed strong natural coordination and resisted electrotactic control, with this conflict actively damaging the leading edge of the tissue. However, reducing preexisting coordination in the tissue by specifically inhibiting E-cadherin–dependent cell–cell adhesion, either by disrupting the formation of cell–cell junctions with E-cadherin–specific antibodies or rapidly dismantling E-cadherin junctions with calcium chelators, significantly improved controllability. Finally, we applied this paradigm of weakening existing coordination to improve control and demonstrate accelerated wound closure in vitro. These results are in keeping with those from diverse, noncellular systems and confirm that endogenous collectivity should be considered as a key quantitative design variable when optimizing external control of collective migration.
43
Chalasani, Sreedevi, and David Matthes. "Investigating the Tissue Specific Expression Patterns of Murine Semaphorins 3C, 4D, 4G, 6A and 7A in Primary Lymphoid Tissues." Microscopy and Microanalysis 7, S2 (August 2001): 76–77. http://dx.doi.org/10.1017/s1431927600026453.
Full textAbstract:
Semaphorins are primarily known for the important role they play in the guidance of growth cones during neuronal development. There is evidence, however, that semaphorins are expressed outside the nervous system as well, suggesting a wider scope for semaphorin function. The overall objective of our study is to identify the functions of semaphorins outside central nervous system especially in T cell development. Some of the 20 semaphorins have been shown to have extra-neural functions that include (for different semaphorins) bone differentiation, promotion of B-cell survival and aggregation, and activation of T-cells. Apart from central nervous system statement of most semaphorins, one semaphorin (CD 100) has transcripts in T cells, B cells, neutrophils, monocytes and granulocytes. EST analysis suggests that other semaphorins are expressed in lymphoid tissues such as thymus, spleen, tonsil, and the interfollicular areas and germinal centers of lymph nodes.Semaphorins have been related to several cell survival mechanisms, immunosuppression and promotion of cell death resistance. in preliminary studies our lab found that viral semaphorins inhibit the migration of human T cells and human SEMA3A can inhibit migration of human neutrophils.
44
Mendi, Ayşegül, Beyza Gökçınar Yağcı, Nurdan Saraç, Mustafa Kızıloğlu, Aysel Uğur, Duygu Uçkan, and Derviş Yılmaz. "The Effects of Hypericum perforatum L. on the Proliferation, Osteogenic Differentiation, and Inflammatory Response of Mesenchymal Stem Cells from Different Niches." Cells Tissues Organs 205, no. 4 (2018): 208–16. http://dx.doi.org/10.1159/000491633.
Full textAbstract:
The aim of this study is to demonstrate and compare the differentiation, proliferation, migration and inflammatory behavior of dental pulp- and bone marrow-derived mesenchymal stem cells (DP-MSCs and BM-MSCs) in response to a Hypericum perforatum ethanol extract. Using xCELLigence, a real-time monitoring system, a dose of 10 µg/mL was found to be the most efficient concentration for vitality. The IC50 values and doubling time were calculated. The results showed that H. perforatum L. was able to accelerate osteogenic differentiation in DP-MSCs, but calcium granulation was impaired in BM-MSCs. H. perforatum L.-induced migration increased when compared to the TNF-α-induced migration in a Transwell migration assay, and the IL-6 cytokine levels between cells also differed. It can be suggested that tissue memory is an important factor in MSCs, and that they differ in their response to external factors. In conclusion, H. perforatum L. can be considered an excellent osteoinductive agent for DP-MSCs but should not be used for BM-MSCs. Tissue-specific osteoinductive agents should be discussed in future studies.
45
Elakad, Omar, Yuchan Li, Natascha Gieser, Sha Yao, Stefan Küffer, Marc Hinterthaner, Bernhard C. Danner, Alexander von Hammerstein-Equord, Philipp Ströbel, and Hanibal Bohnenberger. "Role of Annexin A1 in Squamous Cell Lung Cancer Progression." Disease Markers 2021 (April 17, 2021): 1–10. http://dx.doi.org/10.1155/2021/5520832.
Full textAbstract:
Lung cancer remains the primary cause of cancer-related death worldwide, and its molecular mechanisms of tumor progression need further characterization to improve the clinical management of affected patients. The role of Annexin A1 (ANXA1) in tumorigenesis and cancer progression in general and especially in lung cancer remains to be controversial and seems to be highly tissue specific and inconsistent among tumor initiation, progression, and metastasis. In the current study, we investigated ANXA1 expression in 81 squamous cell lung cancer (SQCLC), 86 pulmonary adenocarcinoma (AC), and 30 small cell lung cancer (SCLC) patient-derived tissue samples and its prognostic impact on patient’s survival. Mechanistically, we analyzed the impact of ANXA1 expression on proliferation and migration of SQCLC cell lines using CRISPR-Cas9 and mammalian overexpression vectors. Strong expression of ANXA1 was significantly correlated to longer overall survival only in SQCLC patients ( P = 0.019 ). Overexpression of ANXA1 promoted proliferation in SQCLC cell lines but suppressed their migration, while knockout of ANXA1 promoted cell migration and suppressed proliferation. In conclusion, ANXA1 expression might elongate patients’ survival by inhibiting tumor cell migration and subsequent metastasis.
46
Hight-Warburton, Willow, and Maddy Parsons. "Regulation of cell migration by α4 and α9 integrins." Biochemical Journal 476, no. 4 (February 28, 2019): 705–18. http://dx.doi.org/10.1042/bcj20180415.
Full textAbstract:
Abstract Integrins are heterodimeric transmembrane receptors that play an essential role in enabling cells to sense and bind to extracellular ligands. Activation and clustering of integrins leads to the formation of focal adhesions at the plasma membrane that subsequently initiate signalling pathways to control a broad range of functional endpoints including cell migration, proliferation and survival. The α4 and α9 integrins form a small sub-family of receptors that share some specific ligands and binding partners. Although relatively poorly studied compared with other integrin family members, emerging evidence suggests that despite restricted cell and tissue expression profiles, these integrins play a key role in the regulation of signalling pathways controlling cytoskeletal remodelling and migration in both adherent and non-adherent cell types. This review summarises the known shared and specific roles for α4 and α9 integrins and highlights the importance of these receptors in controlling cell migration within both homeostatic and disease settings.
47
Pathak, R. K., M. Yokode, R. E. Hammer, S. L. Hofmann, M. S. Brown, J. L. Goldstein, and R. G. Anderson. "Tissue-specific sorting of the human LDL receptor in polarized epithelia of transgenic mice." Journal of Cell Biology 111, no. 2 (August 1, 1990): 347–59. http://dx.doi.org/10.1083/jcb.111.2.347.
Full textAbstract:
The distribution of human low density lipoprotein (LDL) receptors was studied by immunofluorescence and immunoelectron microscopy in epithelial cells of transgenic mice that express high levels of receptors under control of the metallothionein-I promoter. In hepatocytes and intestinal epithelial cells, the receptors were confined to the basal and basolateral surfaces, respectively. Very few LDL receptors were present in coated pits or intracellular vesicles. In striking contrast, in the epithelium of the renal tubule the receptors were present on the apical (lumenal) surface where they appeared to be concentrated at the base of microvilli and were abundant in vesicles of the endocytic recycling pathway. Intravenously administered LDL colloidal gold conjugates bound to the receptors on hepatocyte microvilli and were slowly internalized, apparently through slow migration into coated pits. We conclude that (a) sorting of LDL receptors to the surface of different epithelial cells varies with each tissue; and (b) in addition to a signal for clustering in coated pits, the LDL receptor may contain a signal for retention in noncoated membrane that is manifest in hepatocytes and intestinal epithelial cells, but not in renal epithelial cells or cultured human fibroblasts.
48
JUNGERSEN, G., H. P. FAGERHOLM, P. NANSEN, and L. ERIKSEN. "Development of patent Ascaris suum infections in pigs following intravenous administration of larvae hatched in vitro." Parasitology 119, no. 5 (November 1999): 503–8. http://dx.doi.org/10.1017/s0031182099004928.
Full textAbstract:
The normal tissue migration of Ascaris suum in the pig host involves larval development in the liver accompanied by considerable pathological changes. The vast majority of larvae that reach the small intestine are later expelled by unknown mechanisms. We show that when migration through the liver is bypassed by inoculation of pigs with an intravenous dose of larvae hatched in vitro, the larvae not only complete migration and return to the small intestine, but they also seem to have a greater chance of survival to adulthood. This technique offers new possibilities for studies on specific lung involvement in protective immunity, provides valuable information for the understanding of self cure by larval expulsion, and adds to our understanding of the evolution of migration of Ascaris larvae in tissues.
49
Ward, Stephen G., and Federica M. Marelli-Berg. "Mechanisms of chemokine and antigen-dependent T-lymphocyte navigation." Biochemical Journal 418, no. 1 (January 28, 2009): 13–27. http://dx.doi.org/10.1042/bj20081969.
Full textAbstract:
T-lymphocyte trafficking is targeted to specific organs by selective molecular interactions depending on their differentiation and functional properties. Specific chemokine receptors have been associated with organ-specific trafficking of memory and effector T-cells, as well as the recirculation of naïve T-cells to secondary lymphoid organs. In addition to the acquisition of tissue-selective integrins and chemokine receptors, an additional level of specificity for T-cell trafficking into the tissue is provided by specific recognition of antigen displayed by the endothelium involving the TCRs (T-cell antigen receptors) and co-stimulatory receptors. Activation of PI3K (phosphoinositide 3-kinase) is a robust signalling event shared by most chemokine receptors as well as the TCR and co-stimulatory receptors, contributing to several aspects of T-lymphocyte homing as well as actin reorganization and other components of the general migratory machinery. Accordingly, inhibition of PI3K has been considered seriously as a potential therapeutic strategy by which to combat various T-lymphocyte-dependent pathologies, including autoimmune and inflammatory diseases, as well as to prevent transplant rejection. However, there is substantial evidence for PI3K-independent mechanisms that facilitate T-lymphocyte migration. In this regard, several other signalling-pathway components, including small GTPases, PLC (phospholipase C) and PKC (protein kinase C) isoforms, have also been implicated in T-lymphocyte migration in response to chemokine stimulation. The present review will therefore examine the PI3K-dependent and -independent signal-transduction pathways involved in T-cell migration during distinct modes of T-cell trafficking in response to either chemokines or the TCR and co-stimulatory molecules.
50
Lämmermann, Tim, Jörg Renkawitz, Xunwei Wu, Karin Hirsch, Cord Brakebusch, and Michael Sixt. "Cdc42-dependent leading edge coordination is essential for interstitial dendritic cell migration." Blood 113, no. 23 (June 4, 2009): 5703–10. http://dx.doi.org/10.1182/blood-2008-11-191882.
Full textAbstract:
Abstract Mature dendritic cells (DCs) moving from the skin to the lymph node are a prototypic example of rapidly migrating amoeboid leukocytes. Interstitial DC migration is directionally guided by chemokines, but independent of specific adhesive interactions with the tissue as well as pericellular proteolysis. Instead, the protrusive flow of the actin cytoskeleton directly drives a basal mode of locomotion that is occasionally supported by actomyosin contractions at the trailing edge to propel the cell's rigid nucleus. We here delete the small GTPase Cdc42 in DCs and find that actin flow and actomyosin contraction are still initiated in response to chemotactic cues. Accordingly, the cells are able to polarize and form protrusions. However, in the absence of Cdc42 the protrusions are temporally and spatially dysregulated, which leads to impaired leading edge coordination. Although this defect still allows the cells to move on 2-dimensional surfaces, their in vivo motility is completely abrogated. We show that this difference is entirely caused by the geometric complexity of the environment, as multiple competing protrusions lead to instantaneous entanglement within 3-dimensional extracellular matrix scaffolds. This demonstrates that the decisive factor for migrating DCs is not specific interaction with the extracellular environment, but adequate coordination of cytoskeletal flow.