Academic literature on the topic 'Tissue-specific migration'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources 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.
Journal articles on the topic "Tissue-specific migration"
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.
Dissertations / Theses on the topic "Tissue-specific migration"
1
Heidegger, Simon. "Tissue-specific migration." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-131476.
Full text
2
Neumann, Katrin. "Modulation der gewebespezifischen Migration von CD4+ T-Zellen durch das Lebersinusendothel." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2012. http://dx.doi.org/10.18452/16587.
Full textAbstract:
Die Einwanderung von T-Zellen in ein Gewebe wird durch selektive Wechselwirkungen mit vaskulären Endothelzellen kontrolliert. In der vorliegenden Arbeit wurde der Frage nachgegangen, ob Interaktionen zwischen Lebersinusendothelzellen (LSEC) und CD4+ T-Zellen die gewebespezifische Migration von CD4+ T-Zellen beeinflussen und damit Relevanz für den Verlauf spezifischer Immunantworten haben. Die Präsentation von Antigenen durch zytokinaktivierte LSEC erhöhte die Adhäsion und Transmigration antigenspezifischer CD4+ T-Zellen. Die Daten deuten auf eine Rolle des Lebersinusendothels bei der entzündungsinduzierten, antigenabhängigen Rekrutierung von CD4+ T-Zellen in das Lebergewebe hin. Eine antigenabhängige Aktivierung naiver CD4+ T-Zellen durch LSEC sowie deren Bereitstellung von Retinolsäure induzierte die Expression von darmspezifischen Homingrezeptoren auf CD4+ T-Zellen. LSEC-aktivierte CD4+ T-Zellen migrierten in das Darmgewebe von C57BL/6-Mäusen. Die Ergebnisse legen den Schluss nahe, dass LSEC einen darmspezifischen Homingphänotyp und damit die Migration von in der Leber aktivierten CD4+ T-Zellen in den Darm induzieren. Die Bereitstellung von Chemokinen durch LSEC mittels Transzytose und Immobilisierung verstärkte die Transmigration von CD4+ T-Zellen durch das Endothel. Die Gabe eines Inhibitors der endothelialen Chemokintranszytose während einer Concanavalin A-induzierten Autoimmunhepatitis supprimierte den Verlauf der Hepatitis und führte zu einer verminderten Migration von aktivierten CD4+ T-Zellen in das Lebergewebe. Diese Daten weisen dem Lebersinusendothel eine aktive Beteiligung in der chemokinabhängigen Rekrutierung von CD4+ T-Zellen in die Leber zu. In der vorliegenden Arbeit wurde die Modulation der gewebespezifischen Migration von CD4+ T-Zellen über Antigenpräsentation und Chemokinbereitstellung durch das Lebersinusendothel gezeigt und damit weitere spezifische Aspekte in der Funktion der Leber als immunologisches Organ beschrieben.T-cell immigration into a tissue is controlled by selective interactions with vascular endothelial cells. The present study addressed the question if interactions between liver sinusoidal endothelial cells (LSEC) and CD4+ T cells influence the tissue-specific migration of CD4+ T cells and thus have relevance for the course of specific immune responses. Antigen presentation by cytokine-activated LSEC increased adhesion and transmigration of antigen-specific CD4+ T cells. These results indicate an involvement of LSEC in the inflammation-induced, antigen-specific migration of CD4+ T cells into the liver tissue. Antigen-specific activation of naive CD4+ T cells by LSEC and their supply of retinoic acid induced expression of gut-specific homing receptors on CD4+ T cells. LSEC-activated CD4+ T cells migrated into the intestine of C57BL/6 mice. The findings presented here imply that LSEC induce a gut-specific homing phenotype resulting in migration of liver-activated CD4+ T cells into the intestine. The active supply of chemokines by LSEC via transcytosis and immobilization enhanced transmigration of CD4+ T cells. Administration of an inhibitor of the endothelial chemokine transcytosis during Concanavalin A-induced autoimmune hepatitis suppressed hepatitis and resulted in reduced migration of activated CD4+ T cells into the liver tissue. The data show the impact of LSEC on the chemokine-dependent recruitment of CD4+ T cells into the liver. In the present study the modulation of the tissue-specific migration of CD4+ T cells by LSEC via antigen presentation and supply of chemokines was demonstrated. Thus, additional functional aspects concerning the immunologic functions of the liver were described.
3
Heidegger, Simon [Verfasser]. "Tissue-specific migration : the effect of innate immune activation on lymphocyte homing to the gastrointestinal tract / vorgelegt von Simon Heidegger." 2010. http://d-nb.info/1013149726/34.
Full textBook chapters on the topic "Tissue-specific migration"
1
D’Ambrosio, D., P. Panina-Bordignon, L. Rogge, and F. Sinigaglia. "Molecular Mechanisms of T Helper Cell Differentiation and Tissue-specific Migration." In Current Topics in Microbiology and Immunology, 117–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-60162-0_15.
Full text
2
Saltzman, W. Mark. "Cell Adhesion." In Tissue Engineering. Oxford University Press, 2004. http://dx.doi.org/10.1093/oso/9780195141306.003.0011.
Full textAbstract:
The external surface of the cell consists of a phospholipid bilayer which carries a carbohydrate-rich coat called the glycocalyx; ionizable groups within the glycocalyx, such as sialic acid (N-acetyl neuraminate), contribute a net negative charge to the cell surface. Many of the carbohydrates that form the glycocalyx are bound to membrane-associated proteins. Each of these components— phospholipid bilayer, carbohydrate-rich coat, membrane-associated protein—has distinct physicochemical characteristics and is abundant. Plasma membranes contain ∼50% protein, ∼45% lipid, and ∼5% carbohydrate by weight. Therefore, each component influences cell interactions with the external environment in important ways. Cells can become attached to surfaces. The surface of interest may be geometrically complex (for example, the surface of another cell, a virus, a fiber, or an irregular object), but this chapter will focus on adhesion between a cell and a planar surface. The consequences of cell–cell adhesion are considered further in Chapter 8 (Cell Aggregation and Tissue Equivalents) and Chapter 9 (Tissue Barriers to Molecular and Cellular Transport). The consequences of cell–substrate adhesion are considered further in Chapter 7 (Cell Migration) and Chapter 12 (Cell Interactions with Polymers). Since the growth and function of many tissue-derived cells required attachment and spreading on a solid substrate, the events surrounding cell adhesion are fundamentally important. In addition, the strength of cell adhesion is an important determinant of the rate of cell migration, the kinetics of cell–cell aggregation, and the magnitude of tissue barriers to cell and molecule transport. Cell adhesion is therefore a major consideration in the development of methods and materials for cell delivery, tissue engineering, and tissue regeneration. The most stable and versatile mechanism for cell adhesion involves the specific association of cell surface glycoproteins, called receptors, and complementary molecules in the extracellular space, called ligands. Ligands may exist freely in the extracellular space, they may be associated with the extracellular matrix, or they may be attached to the surface of another cell. Cell–cell adhesion can occur by homophilic binding of identical receptors on different cells, by heterophilic binding of a receptor to a ligand expressed on the surface of a different cell, or by association of two receptors with an intermediate linker. Cell–matrix adhesion usually occurs by heterophilic binding of a receptor to a ligand attached to an insoluble element of the extracellular matrix.
3
Saltzman, W. Mark. "Tissue Barriers to Molecular and Cellular Transport." In Tissue Engineering. Oxford University Press, 2004. http://dx.doi.org/10.1093/oso/9780195141306.003.0014.
Full textAbstract:
Previous chapters have revealed the importance of molecular diffusion in tissue engineering. Molecules—and gradients of molecules—may represent the underlying mechanism of tissue induction and pattern formation (Chapter 3); growth factors—and the rate of delivery of growth factors to a cell surface—can influence the rate of cell proliferation (Chapter 4); chemoattractants can influence the rate and pattern of cell migration within a tissue space (Chapter 7). To think quantitatively about these processes, it is often helpful to think about molecular concentrations and the spatial variations in concentration that produce diffusion fluxes. This idea has been illustrated earlier in the book for specific examples such as bicoid gradient formation in the insect embryo (Section 3.3.4) and ligand diffusion to the cell surface (Section 4.3.2). Some of the basic concepts of molecular transport are also reviewed in Appendix B. But tissues are often heterogeneous structures, formed by the assembly of cells and the accumulation of matrix materials in the extracellular space. The heterogeneous composition of tissues can have a dramatic influence on local rates of molecular movement through the tissue; capillary endothelial cells prevent the diffusion of intravascular proteins into the tissue interstitial space, for example. This chapter discusses this concept and provides quantitative methods for evaluating rates of molecular movement between tissue spaces that are separated by diffusive barriers. In addition, the last section of the chapter shows how this same analysis may be useful when thinking about rates of cellular movement between tissue compartments. In multicellular organisms, thin lipid membranes serve as semipermeable barriers between aqueous compartments. The plasma membrane of the cell separates the cytoplasm from the extracellular space; endothelial cell membranes separate the blood within the vascular space from the rest of the tissue. Properties of the lipid membrane are critically important in regulating the movement of molecules between aqueous spaces. While certain barrier properties of membranes can be attributed to the lipid components, accessory molecules within the cell membrane—particularly transport proteins and ion channels—control the rate of permeation of many solutes.
4
Patricia Rendón-Huerta, Erika, Carlos Abraham García-García, and Luis Felipe Montaño Estrada. "Effect of Helicobacter pylori on Tight Junctions in Gastric Epithelia." In Helicobacter pylori - From First Isolation to 2020 [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96607.
Full textAbstract:
Molecular complexes grouped under the names of tight, adherent or gap junction regulate the flow of water, ions and macromolecules through epithelium paracellular spaces. The main constituents of tight junctions are claudins, a family of 26 different proteins whose expression and distribution are tissue specific but varies in tumors. A change in claudin 1, 3, 4, 5, 6, 7, 9 and 18 expression, that contributes to lose epithelial cohesion, has been associated to enhanced cell proliferation, migration, and invasiveness in gastric neoplastic tissue. Chronic inflammation process induced by H. pylori infection, a major risk factor for gastric cancer development, disrupts tight junctions via CagA gene, Cag pathogenicity island, and VacA, but the effect upon the epithelial barrier of H. pylori lipopolysaccharides or H. pylori-induced up-regulation of mTOR and ERK signaling pathways by microRNA-100 establishes new concepts of proof.
5
Heasman, P. A., and P. J. Waterhouse. "Periodontal diseases in children." In Paediatric Dentistry. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198789277.003.0020.
Full textAbstract:
Periodontal diseases comprise a group of infections that affect the supporting structures of the teeth: marginal and attached gingiva, periodontal ligament, cementum, and alveolar bone. Acute gingival diseases—primarily herpetic gingivostomatitis and necrotizing gingivitis—are ulcerative conditions that result from specific viral and bacterial infection. Chronic gingivitis, however, is a non-specific inflammatory lesion of the marginal gingiva which reflects the bacterial challenge to the host when dental plaque accumulates in the gingival crevice. The development of chronic gingivitis is enhanced when routine oral hygiene practices are impaired. Chronic gingivitis is reversible if effective plaque control measures are introduced. If left untreated, the condition invariably converts to chronic periodontitis, which is characterized by resorption of the supporting connective tissue attachment and apical migration of the junctional epithelia. Slowly progressing, chronic periodontitis affects most of the adult population to a greater or lesser extent, although the early stages of the disease are detected in adolescents. Children are also susceptible to aggressive periodontal diseases that involve the primary and permanent dentitions, and present in localized or generalized forms. These conditions, which are distinct clinical entities affecting otherwise healthy children, must be differentiated from the extensive periodontal destruction that is associated with certain systemic diseases, degenerative disorders, and congenital syndromes. Periodontal tissues are also susceptible to changes that are not, primarily, of an infectious nature. Factitious stomatitis is characterized by self-inflicted trauma to oral soft tissues and the gingiva are invariably involved. Drug-induced gingival enlargement is becoming increasingly prevalent with the widespread use of organ transplant procedures and long-term immunosuppressant therapy. Localized enlargement may occur as a gingival complication of orthodontic treatment. A classification of periodontal diseases in children is given in Table 12.1. Marginal gingival tissues around the primary dentition are more highly vascular and contain fewer connective tissue fibres than tissues around the permanent teeth. The epithelia are thinner with a lesser degree of keratinization, giving an appearance of increased redness that may be interpreted as mild inflammation. Furthermore, the localized hyperaemia that accompanies eruption of the primary dentition can persist, leading to swollen and rounded interproximal papillae and a depth of gingival sulcus exceeding 3mm.
Conference papers on the topic "Tissue-specific migration"
1
Zimnyakov, D. A., V. V. Tuchin, and A. G. Yodh. "Tissue Structure Characterization by Measuring the Specific Correlation Scales of the Scattered Light Fluctuations." In Advances in Optical Imaging and Photon Migration. Washington, D.C.: OSA, 1998. http://dx.doi.org/10.1364/aoipm.1998.atud21.
Full text
2
Ng, Colin, and Amrinder Nain. "Cellular Dynamics on Aligned Fibrous PLGA Scaffolds." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-54014.
Full textAbstract:
Understanding cellular dynamics is fundamental to increasing the healing and regenerative capacity of biomedical scaffolds. The ability to investigate environmental cues and cell-cell interactions in vitro with successful translation to in vivo therapies will enhance many tissue engineering technologies. Understanding the dynamics of a cell in response to external mechanical stimuli can help achieve directed cellular migration by varying cellular environment geometries. Customized scaffolds can then be designed to achieve desired cellular migration rates, cell-cell interaction pathways, increased proliferation and directed cellular differentiation platforms to achieve tissue engineering specific goals. In this study, a unique fiber manufacturing platform known as STEP (Spinneret-based Tunable Engineered Parameters) is used to create and manipulate geometrical cues for cellular migration. The cell’s reaction to these geometric cues provides valuable insight into cellular behavior, which can be used to determine the optimal engineered microenvironment. We envision that studying cellular behavior on STEP enabled customized scaffolds will aid in the design and fabrication of accurate mechanistic environments for different cell types which can then be coupled with chemical cues to achieve desired results.
3
Pryse, Kenneth M., Teresa M. Abney, Guy M. Genin, and Elliot L. Elson. "Probing Cytoskeletal Mechanics Using Biochemical Inhibitors." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19451.
Full textAbstract:
Quantifying the mechanics of the cytoskeletons of living cells is important for understanding several physiologic and pathologic cellular functions, such as wound healing and cellular migration in cancer. Our laboratory develops three-dimensional tissue constructs for assaying cytoskeletal mechanics in controlled conditions. These tissue constructs consist of defined components such as chick embryo fibroblasts and reconstituted rat tail collagen; fibroblasts remodel the collagen extracellular matrix (ECM) and develop a structural environment representative of that which would exist in a natural tissue. Our protocol for quantifying the microscale mechanics of the proteins that comprise the cytoskeleton involves mechanical testing of a tissue construct first in a bath that contains nutrition medium to support the active physiologic functioning of the cells, and next in the presence of inhibitors that selectively eliminate specific cytoskeletal structures. By solving an inverse homogenization problem, the mechanical functioning of these proteins at the cellular level can be estimated. Here, we present a combination of mechanical testing and imaging results to quantify the effects of specific inhibitors on cytoskeletal and extracellular matrix form and function.
4
Wasi, S., S. Juodvalkis, P. Alles, and J. E. Aubin. "STUDIES ON THE DIRECT PROTEOLYTIC ACTION OF HUMAN TISSUE PLASMINOGEN ACTIVATOR ON HUMAN FIBRONECTIN AND VITRONECTIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644376.
Full textAbstract:
The ability of cells to make or break specific attachments to extracellular matrix (ECM) and other cells is important in cell migration, proliferation and wound repair. Specific attachment proteins believed to be involved in mediating these interactions comprise functional domains joined by protease sensitive segments. Proteases can conceivably modulate cellular interactions by releasing functional domains from parent molecules. Tissue plasminogen activator (t-pA) is known to participate in various pathophysiological processes. That t-pA may also act directly on structural proteins has not been investigated. We have studied the direct proteolytic action of melanoma t-pA on fibronectin (FN), vitronectin (VN) and laminin (LN). These were incubated with t-pA for 0 to 48 h in 50 mM Tris HCi, pH 7.4. The cleavage products were separated on polyacrylamide slab gels and blotted onto nitrocellulose strips. FN and VN fragments with cell attachment properties were identified by incubating the strips with human gingiva fibroblasts and staining with Amido black. Monoclonal antibodies to FN were used to identify heparin, cell and gelatin binding fragments. VN was converted to a major 55 Kd product as a function of time. Lower molecular weight species migrating at 45 Kd, 30 Kd and 15 Kd positions were also identified. Most of these fragments possessed cell attachment properties. LN became susceptible to t-pA digestion after dénaturation with H2O2. The catalytic activity of t-pA could be inhibited in the presence of nitrophenyl-p-guinidino benzoate (a synthetic inhibitor of plasminogen activator), whereas O-phenanthroline (a metalloprotease inhibitor), α 2-antiplasmin and trasylol had no effect. A monoclonal IgG preparation (HI 72 A1, kindly provided by Dr. David J. Loskutoff) that specifically inhibits t-pA also inhibited the protelyotic action of t-pA on FN. These data suggest that direct proteolytic action of t-pA on adhesive proteins may modulate cellular behaviour in various normal and pathological conditions which involve dynamic interactions between cells and ECM and where plasminogen activator levels are elevated either transiently or permanently, for example during tissue remodelling, wound-related repair and thrombolytic therapy.
5
Wong, Henry C., and William C. Tang. "Effects of Friction Coefficient and Receptor Number on Cell-Substrate Interactions During Migration." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19323.
Full textAbstract:
Biological tissues are composed of cells that adhere to the extracellular matrix (ECM) via cell-surface integrin receptors that bind to specific proteins, such as fibronectin, embedded in the matrix. In this manner, the ECM functions as a structural support for the attached cells, and mechanical forces are able to be transmitted from the cell to the ECM and vice versa [1]. Cell migration, a process that is highly dependent on these mechanical interactions, is important for many normal biological processes and diseases that occur in the human body, which include embryonic development, immune response, would healing, and cancer invasion [2]. Though many continuum models of cell migration have been proposed, there is still a need for a model that can be used to quantitatively understand the mechanical factors that can influence the movement of a cell on a substrate. This would be invaluable to the research areas of tissue engineering as well as cancer metastasis. We utilized a finite element model to elucidate the mechanism of cell-substrate interactions for a cell that consistently migrates in a single direction. Our model follows the approach taken by Gracheva and Othmer [2], but we extended their model to describe two-dimensional plane strain behavior.
6
Jabbari, Esmaiel, David N. Rocheleau, Weijie Xu, and Xuezhong He. "Fabrication of Biomimetic Scaffolds With Well-Defined Pore Geometry by Fused Deposition Modeling." In ASME 2007 International Manufacturing Science and Engineering Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/msec2007-31011.
Full textAbstract:
It is well established that the pore size and distribution affect the rate of cell migration and the extent of extracellular matrix formation. The objective of this work was to develop a process for fabrication of biodegradable and shape-specific polymeric scaffolds with well-defined pore geometry, functionalized with covalently attached bioactive peptides, for applications in tissue regeneration. We have used the Fused Deposition Modeling (FDM) RP technology to fabricate degradable and functional scaffolds with well-defined pore geometry. Computer aided design (CAD) using SolidWorks was used to create models of the cubic orthogonal geometry. The models were used to create the machine codes necessary to build the scaffolds with FDM with wax as the build material. A novel biodegradable in-situ crosslinkable macromer, poly(lactide-co-glycolide fumarate) or PLGF, mixed with reactive functional peptides was infused in the scaffold and allowed to crosslink. The scaffold was then immersed in a hydrocarbon solvent to remove the wax, leaving just the PLGF behind as the support material dissolved. The pore morphology of the PLGF scaffold was imaged with micro-computed tomography and scanning electron microscopy. Cellular function in the PLFG scaffolds with well-defined pore geometry was studied with bone marrow stromal cells isolated from rats. Results demonstrate that the scaffolds support homogeneous formation of mineralized tissue.
7
Schleuning, W. D. "THE BIOCHEMISTRY AND CELL BIOLOGY OF SINGLE CHAIN UROKINASE TYPE PLASMINOGEN ACTIVATOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642956.
Full textAbstract:
Urokinase was discovered in the late nineteenth century, as an enzymatic principle in urine, that initiates the dissolution of blood clots. The basis of this phenomenon was recognized more than fifty years ago as the activation of plasminogen, the precursor of a tryptic protease, then known as profibrinolysin. Despite this long history, detailed data on the biochemistry of plasminogen activation have only become available recently. Urokinase (now designated urokinase-type plasminogen activator : u-PA) is synthesized and secreted as a single chain polypeptide (Mr-: 53,000) by many cell types. Single chain u-PA (scu-PA) is with equal justification called prourokinase (pro-u-PA), notwithstanding its low catalytic activity for synthetic peptide substrates and plasminogen, as most proenzymes of proteases display a certain degree of activity. The structure of pro-u-PA has been elucidated by protein and cDNA sequencing. It consists of three domains, exhibiting characteristic homology to other proteins: a serine protease domain, homologous to trypsin, chymotrypsin and elastase; a kringle domain, likewise found in prothrombin, plasminogen, tissue-type plasminogen activator (t-PA) and Factor XII; and an epidermal growth factor (EGF)-like domain, found in many other proteins, including certain clotting factors. Pro-u-PA is activated by the cleavage of its LYS158-Ile159 h1 bY either plasmin or kallikrein. This cleavage leads to a high increase of Kcat values with respect to both plasminogen and synthetic peptide substrates, but apparently to a reduction of its affinity to plasminogen. Thrartoin inactivates pro-u-PA irreversibly by the cleavage of the Arg156-Phe157 bond. U-PA but not pro-u-PA rapidly forms ccnplexes with plasminogen activator inhibitors (PAI)-l and PAI-2: second order rate constants Kass are respectively > 107 and 0.9xl06 (M-11sec-1). Unknown enzymes process pro-u-PA and u-PA to low molecular weight (LMW) pro-u-PA and LMW u-PA (Mr: 33,000) by cutting off a fragment consisting of the kr ingle and the EGF—like region. Pro—u—PA mediated plasminogen activation is fibrin dependent in vivo, and to a certain degree in vitro. Hie biochemical basis of this fibrin specificity is at present uncertain, although there are reports indicating that it may require polyvalent cations. Through its EGF-like region HMW pro-u-PA and HMW u-PA are capable of binding to specific membrane protein receptors which are found on many cells. Thus, u-PA activity may be restricted to the cell surface. According to a recent report, binding of u—PA to the receptor may also mediate signal transduction in auto- or paracrine growth control. In cells permissive for the respective pathways, pro-u-PA gene transcription is stimulated by mechanisms of signal transduction, that include the cAMP, the tyrosine specific kinase and the protein kinase C dependent pathways. Glucocorticoid hormones downregulate pro-u-PA gene transcription in cells where the gene is canstitutively expressed. Although different cells vary greatly in their response to agents that stimulate urokinase biosynthesis, growth factors and other mitogens are in many cases effective inducers. Significantly elevated levels of u-PA are also found in many malignant tissues. These findings and many others suggest that plasminogen activation by u-PA provides localized extracellular matrix degradation which is required for invasive growth, cell migration and other forms of tissue remodelling. Fibrin represents in this view only a variant of an extracellular matrix, which is provided through the clotting system in the case of an emergency.