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Evaluation of extracellular matrices and proteinase interactions in bovine and porcine endodermal cell migration in vitroSchilperoort-Haun, Kelly Rae 28 March 1997 (has links)
Graduation date: 1997
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Functional analyses of type IIA procollagen in embryo development /Leung, Wai-lun, Alan. January 2006 (has links)
Thesis (Ph. D.)--University of Hong Kong, 2006.
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Biomechanics of common carotid arteries from mice heterozygous for mgR, the most common mouse model of Marfan syndromeTaucer, Anne Irene 15 May 2009 (has links)
Marfan syndrome, affecting approximately one out of every 5,000 people, is
characterized by abnormal bone growth, ectopia lentis, and often-fatal aortic dilation and
dissection. The root cause is a faulty extracellular matrix protein, fibrillin-1, which
associates with elastin in many tissues. Common carotids from wild-type controls and
mice heterozygous for the mgR mutation, the most commonly used mouse model of
Marfan syndrome, were studied in a biaxial testing device. Mechanical data in the form
of pressure-diameter and force-stretch tests in both the active and passive states were
collected, as well data on the functional responses to phenylephrine, carbamylcholine
chloride, and sodium nitroprusside. Although little significant difference was found
between the heterozygous and wild-type groups in general, the in vivo stretch for both
groups was significantly different from previously studied mouse vessels. Although the
two groups do not exhibit significant differences, this study comprises a control group
for future work with mice homozygous for mgR, which do exhibit Marfan-like
symptoms. As treatment of Marfan syndrome improves, more Marfan patients will
survive and age, increasing the likelihood that they will develop many of the vascular complications affecting the normal population, including hypertension and
atherosclerosis. Therefore, it is imperative to gather biomechanical data from the Marfan
vasculature so that clinicians may predict the effects of vascular complications in Marfan
patients and develop appropriate methods of treatment.
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Integrated biomechanical model of cells embedded in extracellular matrixMuddana, Hari Shankar 15 May 2009 (has links)
Nature encourages diversity in life forms (morphologies). The study of morphogenesis
deals with understanding those processes that arise during the embryonic development
of an organism. These processes control the organized spatial distribution of cells,
which in turn gives rise to the characteristic form for the organism. Morphogenesis
is a multi-scale modeling problem that can be studied at the molecular, cellular, and
tissue levels.
Here, we study the problem of morphogenesis at the cellular level by introducing
an integrated biomechanical model of cells embedded in the extracellular matrix.
The fundamental aspects of mechanobiology essential for studying morphogenesis at
the cellular level are the cytoskeleton, extracellular matrix (ECM), and cell adhesion.
Cells are modeled using tensegrity architecture. Our simulations demonstrate cellular
events, such as differentiation, migration, and division using an extended tensegrity
architecture that supports dynamic polymerization of the micro-filaments of the cell.
Thus, our simulations add further support to the cellular tensegrity model. Viscoelastic
behavior of extracellular matrix is modeled by extending one-dimensional
mechanical models (by Maxwell and by Voigt) to three dimensions using finite element
methods. The cell adhesion is modeled as a general Velcro-type model. We
integrated the mechanics and dynamics of cell, ECM, and cell adhesion with a geometric
model to create an integrated biomechanical model. In addition, the thesis discusses various computational issues, including generating the finite element mesh,
mesh refinement, re-meshing, and solution mapping.
As is known from a molecular level perspective, the genetic regulatory network of
the organism controls this spatial distribution of cells along with some environmental
factors modulating the process. The integrated biomechanical model presented here,
besides generating interesting morphologies, can serve as a mesoscopic-scale platform
upon which future work can correlate with the underlying genetic network.
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Model substrates for mechanistic studies of cell-matrix interactions /Houseman, Benjamin Thomas. January 2001 (has links)
Thesis (Ph. D.)--University of Chicago, Dept. of Chemistry, June 2001. / Includes bibliographical references. Also available on the Internet.
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Tissue engineering cellularized silk-based ligament analoguesSell, Scott. January 1900 (has links)
Thesis (Ph.D.)--Virginia Commonwealth University, 2009. / Prepared for: Dept. of Biomedical Engineering. Title from resource description page. Includes bibliographical references.
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The effect of adipokines on collagens and matrix metalloproteinases in rat cardiac cells /Wong, Man Chee Maggie. January 2007 (has links)
Thesis (M.Sc.)--York University, 2007. Graduate Programme in Biology. / Typescript. Includes bibliographical references (leaves 119-133). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:MR38842
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Cellular and extracellular matrix characteristics of canine chondrocytes in pathologic conditionsKuroki, Keiichi, January 2003 (has links)
Thesis (Ph. D.)--University of Missouri--Columbia, 2003. / Typescript. Vita. Includes bibliographical references.
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Cellular and extracellular matrix characteristics of canine chondrocytes in pathologic conditions /Kuroki, Keiichi, January 2003 (has links)
Thesis (Ph. D.)--University of Missouri--Columbia, 2003. / "May 2003." Typescript. Vita. Includes bibliographical references.
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Extracellular matrix mechanics regulate cell signaling and migratory potential in cancerSrivastava, Jaya, active 2012 14 November 2013 (has links)
The objective of the presented research is to examine the relationship between the cellular microenvironment and biochemical response of metastatic cells. Clinically recognized as a trait of cancer progression, the cellular microenvironment can have variable and distinct mechanical properties that are processed via cellular mechanosensing, resulting in a cellular biochemical response. A range of studies investigating the interactions between the cellular micromechanical environment and the cell's molecular response during disease progression have been made, yet remain absent of quantitative characterization of many of these coordinated responses. The fundamental inquiry that drives the following research attempts to elucidate how a cell perceives the physical microenvironment and converts that signal to a biochemical response. With the goal of providing insight to such responses, the presented research seeks to elucidate the following questions: (1) What are the integrated effects of ECM stiffness, ECM architecture, and breast cancer cell metastatic potential on cell migration? (2) How does endogenous tissue transglutaminase (tTG) cross-linking of the ECM scaffold effect ECM mechanical properties? (3) How does the architecture and stiffness of the extracellular matrix (ECM) effect the systems-level cellular migration and signaling response? (4) What are the integrated effects of ECM architecture and the targeted knockdown of integrin [beta]1 and MT1-MMP on cellular metastatic potential? The presented research utilizes an interdisciplinary approach, integrating experimental mechanics, biochemical analysis, cellular biology techniques, covalent chemistry, and various microscopy techniques, to investigate these events. In short, cancerous cells are cultured atop or within synthetic collagen type I ECMs of varying mechanical stiffness and structure. These cells are subsequently analyzed by molecular analysis and immunoassays, including quantitative PCR, Western blotting, and gelatin zymography, to acquire measures of the cellular response to perturbations of micromechanical environment. Time-lapse microscopy experiments and subsequent image analyses enable observations of cellular migratory potential through synthetic ECMs. Results indicate that cooperative synergy between ECM properties, cell-matrix adhesion, and pericellular proteolysis drive cell migratory potential of highly invasive tumorigenic cell populations. Collectively, these findings contribute to the cancer biology and mechanobiology fields by systematically extending current insights of matrix mechanics, cellular signaling, and cellular migratory potential in cancer. / text
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