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Inhomogeneities in 3D Collagen Matrices Impact Matrix Mechanics and Cancer Cell MigrationHayn, Alexander, Fischer, Tony, Mierke, Claudia Tanja 03 April 2023 (has links)
Cell motility under physiological and pathological conditions including malignant
progression of cancer and subsequent metastasis are founded on environmental
confinements. During the last two decades, three-dimensional cell migration has been
studied mostly by utilizing biomimetic extracellular matrix models. In the majority of
these studies, the in vitro collagen scaffolds are usually assumed to be homogenous,
as they consist commonly of one specific type of collagen, such as collagen type I,
isolated from one species. These collagen matrices should resemble in vivo extracellular
matrix scaffolds physiologically, however, mechanical phenotype and functional reliability
have been addressed poorly due to certain limitations based on the assumption
of homogeneity. How local variations of extracellular matrix structure impact matrix
mechanics and cell migration is largely unknown. Here, we hypothesize that local
inhomogeneities alter cell movement due to alterations in matrix mechanics, as they
frequently occur in in vivo tissue scaffolds and were even changed in diseased tissues.
To analyze the effect of structural inhomogeneities on cell migration, we used a mixture
of rat tail and bovine dermal collagen type I as well as pure rat and pure bovine collagens
at four different concentrations to assess three-dimensional scaffold inhomogeneities.
Collagen type I from rat self-assembled to elongated fibrils, whereas bovine collagen
tended to build node-shaped inhomogeneous scaffolds. We have shown that the
elastic modulus determined with atomic force microscopy in combination with pore size
analysis using confocal laser scanning microscopy revealed distinct inhomogeneities
within collagen matrices. We hypothesized that elastic modulus and pore size govern
cancer cell invasion in three-dimensional collagen matrices. In fact, invasiveness of three
breast cancer cell types is altered due to matrix-type and concentration indicating that
these two factors are crucial for cellular invasiveness. Our findings revealed that local
matrix scaffold inhomogeneity is another crucial parameter to explain differences in
cell migration, which not solely depended on pore size and stiffness of the collagen
matrices. With these three distinct biophysical parameters, characterizing structure
and mechanics of the studied collagen matrices, we were able to explain differences
in the invasion behavior of the studied cancer cell lines in dependence of the used
collagen model.
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The Pertinent Role of Cell and Matrix Mechanics in Cell Adhesion and MigrationMierke, Claudia Tanja 03 April 2023 (has links)
No description available.
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Viscoelasticity Acts as a Marker for Tumor Extracellular Matrix CharacteristicsMierke, Claudia Tanja 03 April 2023 (has links)
Biological materials such as extracellular matrix scaffolds, cancer cells, and tissues are
often assumed to respond elastically for simplicity; the viscoelastic response is quite
commonly ignored. Extracellular matrix mechanics including the viscoelasticity has turned
out to be a key feature of cellular behavior and the entire shape and function of healthy and
diseased tissues, such as cancer. The interference of cells with their local
microenvironment and the interaction among different cell types relies both on the
mechanical phenotype of each involved element. However, there is still not yet clearly
understood how viscoelasticity alters the functional phenotype of the tumor extracellular
matrix environment. Especially the biophysical technologies are still under ongoing
improvement and further development. In addition, the effect of matrix mechanics in
the progression of cancer is the subject of discussion. Hence, the topic of this review is
especially attractive to collect the existing endeavors to characterize the viscoelastic
features of tumor extracellular matrices and to briefly highlight the present frontiers in
cancer progression and escape of cancers from therapy. Finally, this review article
illustrates the importance of the tumor extracellular matrix mechano-phenotype,
including the phenomenon viscoelasticity in identifying, characterizing, and treating
specific cancer types.
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The Collagen Receptor Discoidin Domain Receptor 1b Enhances Integrin β1-Mediated Cell Migration by Interacting With Talin and Promoting Rac1 ActivationBorza, Corina M., Bolas, Gema, Zhang, Xiuqi, Browning Monroe, Mary Beth, Zhang, Ming-Zhi, Meiler, Jens, Skwark, Marcin J., Harris, Raymond C., Lapierre, Lynne A., Goldenring, James R., Hook, Magnus, Rivera, Jose, Brown, Kyle L., Leitinger, Birgit, Tyska, Matthew J., Moser, Markus, Böttcher, Ralph T., Zent, Roy, Pozzi, Ambra 03 April 2023 (has links)
Integrins and discoidin domain receptors (DDRs) 1 and 2 promote cell adhesion and
migration on both fibrillar and non fibrillar collagens. Collagen I contains DDR and integrin
selective binding motifs; however, the relative contribution of these two receptors in
regulating cell migration is unclear. DDR1 has five isoforms (DDR1a-e), with most cells
expressing the DDR1a and DDR1b isoforms. We show that human embryonic kidney 293
cells expressing DDR1b migrate more than DDR1a expressing cells on DDR selective
substrata as well as on collagen I in vitro. In addition, DDR1b expressing cells show
increased lung colonization after tail vein injection in nude mice. DDR1a and DDR1b differ
from each other by an extra 37 amino acids in the DDR1b cytoplasmic domain.
Interestingly, these 37 amino acids contain an NPxY motif which is a central control
module within the cytoplasmic domain of β integrins and acts by binding scaffold proteins,
including talin. Using purified recombinant DDR1 cytoplasmic tail proteins, we show that
DDR1b directly binds talin with higher affinity than DDR1a. In cells, DDR1b, but not DDR1a,
colocalizes with talin and integrin β1 to focal adhesions and enhances integrin β1-mediated
cell migration. Moreover, we show that DDR1b promotes cell migration by enhancing Rac1
activation. Mechanistically DDR1b interacts with the GTPase-activating protein (GAP)
Breakpoint cluster region protein (BCR) thus reducing its GAP activity and enhancing Rac
activation. Our study identifies DDR1b as a major driver of cell migration and talin and BCR
as key players in the interplay between integrins and DDR1b in regulating cell migration.
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The Presence of Extracellular Matrix Alters the Chondrocyte Response to Endoplasmic Reticulum StressNugent, Ashleigh Elizabeth 19 April 2010 (has links)
No description available.
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Functional and Structural Analysis of Decellularized Liver Tissue Matrix, with Potential Applications in Cancer Tissue EngineeringHansen, Ryan 30 August 2017 (has links)
No description available.
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Immuno-nanotherapeutics to Inhibit Macrophage Polarization for Non-Small-Cell Lung CancersSeshadri, Dhruv Ramakrishna January 2017 (has links)
No description available.
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The role of transforming growth factor beta-extracellular matrix signaling in skeletal muscle growth and developmentLi, Xuehui 10 September 2008 (has links)
No description available.
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FINITE ELEMENT MODELING OF COLLAGEN FIBERS IN THE MECHANICAL INTERACTION BETWEEN CELLS AND THE EXTRACELLULAR MATRIXMa, Xiaoyue 24 August 2012 (has links)
No description available.
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Native extracellular matrix: a new scaffolding platform for repair of damaged muscleTeodori, Laura, Costa, Alessandra, Marzio, Rosa, Perniconi, Barbara, Coletti, Dario, Adamo, Sergio, Gupta, Bhuvanesh, Tarnok, Attila 03 August 2022 (has links)
Effective clinical treatments for volumetric muscle loss resulting from traumatic injury or resection of a large amount of muscle mass are not available to date. Tissue engineering may represent an alternative treatment approach. Decellularization of tissues and whole organs is a recently introduced platform technology for creating scaffolding materials for tissue engineering and regenerative medicine. The muscle stem cell niche is composed of a three-dimensional architecture of fibrous proteins, proteoglycans, and glycosaminoglycans, synthesized by the resident cells that form an intricate extracellular matrix (ECM) network in equilibrium with the surrounding cells and growth factors. A consistent body of evidence indicates that ECM proteins regulate stem cell differentiation and renewal and are highly relevant to tissue engineering applications. The ECM also provides a supportive medium for blood or lymphatic vessels and for nerves. Thus, the ECM is the nature's ideal biological scaffold material. ECM-based bioscaffolds can be recellularized to create potentially functional constructs as a regenerative medicine strategy for organ replacement or tissue repopulation. This article reviews current strategies for the repair of damaged muscle using bioscaffolds obtained from animal ECM by decellularization of small intestinal submucosa (SIS), urinary bladder mucosa (UB), and skeletal muscle, and proposes some innovative approaches for the application of such strategies in the clinical setting.
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