Extracellular Matrix

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Ruiyun Zhang - One of the best experts on this subject based on the ideXlab platform.

  • synthetic nano scale fibrous Extracellular Matrix
    Journal of Biomedical Materials Research, 1999
    Co-Authors: Peter X, Ruiyun Zhang
    Abstract:

    Biodegradable polymers have been widely used as scaffolding materials to regenerate new tissues. To mimic natural Extracellular Matrix architecture, a novel highly po- rous structure, which is a three-dimensional interconnected fibrous network with a fiber diameter ranging from 50 to 500 nm, has been created from biodegradable aliphatic polyes- ters in this work. A porosity as high as 98.5% has been achieved. These nano-fibrous matrices were prepared from the polymer solutions by a procedure involving thermally induced gelation, solvent exchange, and freeze-drying. The effects of polymer concentration, thermal annealing, solvent exchange, and freezing temperature before freeze-drying on the nano-scale structures were studied. In general, at a high gelation temperature, a platelet-like structure was formed. At a low gelation temperature, the nano-fibrous structure was formed. Under the conditions for nano-fibrous Matrix formation, the average fiber diameter (160-170 nm) did not change statistically with polymer concentration or gelation temperature. The porosity decreased with polymer concen- tration. The mechanical properties (Young's modulus and tensile strength) increased with polymer concentration. A surface-to-volume ratio of the nano-fibrous matrices was two to three orders of magnitude higher than those of fi- brous nonwoven fabrics fabricated with the textile technol- ogy or foams fabricated with a particulate-leaching tech- nique. This synthetic analogue of natural Extracellular ma- trix combined the advantages of synthetic biodegradable polymers and the nano-scale architecture of Extracellular Matrix, and may provide a better environment for cell at- tachment and function. © 1999 John Wiley & Sons, Inc. J Biomed Mater Res, 46, 60-72, 1999.

  • Synthetic nano-scale fibrous Extracellular Matrix
    Journal of Biomedical Materials Research, 1999
    Co-Authors: P. X. Ma, Ruiyun Zhang
    Abstract:

    Biodegradable polymers have been widely used as scaffolding materials to regenerate new tissues. To mimic natural Extracellular Matrix architecture, a novel highly porous structure, which is a three-dimensional interconnected fibrous network with a fiber diameter ranging from 50 to 500 nm, has been created from biodegradable aliphatic polyesters in this work. A porosity as high as 98.5% has been achieved. These nano-fibrous matrices were prepared from the polymer solutions by a procedure involving thermally induced gelation, solvent exchange, and freeze-drying. The effects of polymer concentration, thermal annealing, solvent exchange, and freezing temperature before freeze-drying on the nano-scale structures were studied. In general, at a high gelation temperature, a platelet-like structure was formed. At a low gelation temperature, the nano-fibrous structure was formed. Under the conditions for nano-fibrous Matrix formation, the average fiber diameter (160-170 nm) did not change statistically with polymer concentration or gelation temperature. The porosity decreased with polymer concentration. The mechanical properties (Young's modulus and tensile strength) increased with polymer concentration. A surface-to-volume ratio of the nano-fibrous matrices was two to three orders of magnitude higher than those of fibrous nonwoven fabrics fabricated with the textile technology or foams fabricated with a particulate-leaching technique. This synthetic analogue of natural Extracellular Matrix combined the advantages of synthetic biodegradable polymers and the nano-scale architecture of Extracellular Matrix, and may provide a better environment for cell attachment and function.

Elaine P S Gee - One of the best experts on this subject based on the ideXlab platform.

  • control of lung vascular permeability and endotoxin induced pulmonary oedema by changes in Extracellular Matrix mechanics
    Nature Communications, 2013
    Co-Authors: Akiko Mammoto, Tadanori Mammoto, Mathumai Kanapathipillai, Chong Wing Yung, Elisabeth Jiang, Amanda Jiang, Kristopher A Lofgren, Elaine P S Gee
    Abstract:

    Increased vascular permeability contributes to many diseases, including acute respiratory distress syndrome, cancer and inflammation. Most past work on vascular barrier function has focused on soluble regulators, such as tumour-necrosis factor-α. Here we show that lung vascular permeability is controlled mechanically by changes in Extracellular Matrix structure. Our studies reveal that pulmonary vascular leakage can be increased by altering Extracellular Matrix compliance in vitro and by manipulating lysyl oxidase-mediated collagen crosslinking in vivo. Either decreasing or increasing Extracellular Matrix stiffness relative to normal levels disrupts junctional integrity and increases vascular leakage. Importantly, endotoxin-induced increases of vascular permeability are accompanied by concomitant increases in Extracellular Matrix rigidity and lysyl oxidase activity, which can be prevented by inhibiting lysyl oxidase activity. The identification of lysyl oxidase and the Extracellular Matrix as critical regulators of lung vascular leakage might lead to the development of new therapeutic approaches for the treatment of pulmonary oedema and other diseases caused by abnormal vascular permeability.

  • control of lung vascular permeability and endotoxin induced pulmonary oedema by changes in Extracellular Matrix mechanics
    Nature Communications, 2013
    Co-Authors: Akiko Mammoto, Tadanori Mammoto, Mathumai Kanapathipillai, Chong Wing Yung, Elisabeth Jiang, Amanda Jiang, Kristopher A Lofgren, Elaine P S Gee
    Abstract:

    Increased vascular permeability contributes to many diseases, including acute respiratory distress syndrome, cancer and inflammation. Most past work on vascular barrier function has focused on soluble regulators, such as tumour-necrosis factor-α. Here we show that lung vascular permeability is controlled mechanically by changes in Extracellular Matrix structure. Our studies reveal that pulmonary vascular leakage can be increased by altering Extracellular Matrix compliance in vitro and by manipulating lysyl oxidase-mediated collagen crosslinking in vivo. Either decreasing or increasing Extracellular Matrix stiffness relative to normal levels disrupts junctional integrity and increases vascular leakage. Importantly, endotoxin-induced increases of vascular permeability are accompanied by concomitant increases in Extracellular Matrix rigidity and lysyl oxidase activity, which can be prevented by inhibiting lysyl oxidase activity. The identification of lysyl oxidase and the Extracellular Matrix as critical regulators of lung vascular leakage might lead to the development of new therapeutic approaches for the treatment of pulmonary oedema and other diseases caused by abnormal vascular permeability. Vascular permeability is increased by inflammation and in disorders such as acute respiratory distress syndrome. Mammoto et al. show that lung vascular permeability is controlled by the stiffness of the Extracellular Matrix and identify lysyl oxidase as a regulator of vascular leakage in pulmonary oedema in mice.

Chong Wing Yung - One of the best experts on this subject based on the ideXlab platform.

  • control of lung vascular permeability and endotoxin induced pulmonary oedema by changes in Extracellular Matrix mechanics
    Nature Communications, 2013
    Co-Authors: Akiko Mammoto, Tadanori Mammoto, Mathumai Kanapathipillai, Chong Wing Yung, Elisabeth Jiang, Amanda Jiang, Kristopher A Lofgren, Elaine P S Gee
    Abstract:

    Increased vascular permeability contributes to many diseases, including acute respiratory distress syndrome, cancer and inflammation. Most past work on vascular barrier function has focused on soluble regulators, such as tumour-necrosis factor-α. Here we show that lung vascular permeability is controlled mechanically by changes in Extracellular Matrix structure. Our studies reveal that pulmonary vascular leakage can be increased by altering Extracellular Matrix compliance in vitro and by manipulating lysyl oxidase-mediated collagen crosslinking in vivo. Either decreasing or increasing Extracellular Matrix stiffness relative to normal levels disrupts junctional integrity and increases vascular leakage. Importantly, endotoxin-induced increases of vascular permeability are accompanied by concomitant increases in Extracellular Matrix rigidity and lysyl oxidase activity, which can be prevented by inhibiting lysyl oxidase activity. The identification of lysyl oxidase and the Extracellular Matrix as critical regulators of lung vascular leakage might lead to the development of new therapeutic approaches for the treatment of pulmonary oedema and other diseases caused by abnormal vascular permeability.

  • control of lung vascular permeability and endotoxin induced pulmonary oedema by changes in Extracellular Matrix mechanics
    Nature Communications, 2013
    Co-Authors: Akiko Mammoto, Tadanori Mammoto, Mathumai Kanapathipillai, Chong Wing Yung, Elisabeth Jiang, Amanda Jiang, Kristopher A Lofgren, Elaine P S Gee
    Abstract:

    Increased vascular permeability contributes to many diseases, including acute respiratory distress syndrome, cancer and inflammation. Most past work on vascular barrier function has focused on soluble regulators, such as tumour-necrosis factor-α. Here we show that lung vascular permeability is controlled mechanically by changes in Extracellular Matrix structure. Our studies reveal that pulmonary vascular leakage can be increased by altering Extracellular Matrix compliance in vitro and by manipulating lysyl oxidase-mediated collagen crosslinking in vivo. Either decreasing or increasing Extracellular Matrix stiffness relative to normal levels disrupts junctional integrity and increases vascular leakage. Importantly, endotoxin-induced increases of vascular permeability are accompanied by concomitant increases in Extracellular Matrix rigidity and lysyl oxidase activity, which can be prevented by inhibiting lysyl oxidase activity. The identification of lysyl oxidase and the Extracellular Matrix as critical regulators of lung vascular leakage might lead to the development of new therapeutic approaches for the treatment of pulmonary oedema and other diseases caused by abnormal vascular permeability. Vascular permeability is increased by inflammation and in disorders such as acute respiratory distress syndrome. Mammoto et al. show that lung vascular permeability is controlled by the stiffness of the Extracellular Matrix and identify lysyl oxidase as a regulator of vascular leakage in pulmonary oedema in mice.

Mathumai Kanapathipillai - One of the best experts on this subject based on the ideXlab platform.

  • control of lung vascular permeability and endotoxin induced pulmonary oedema by changes in Extracellular Matrix mechanics
    Nature Communications, 2013
    Co-Authors: Akiko Mammoto, Tadanori Mammoto, Mathumai Kanapathipillai, Chong Wing Yung, Elisabeth Jiang, Amanda Jiang, Kristopher A Lofgren, Elaine P S Gee
    Abstract:

    Increased vascular permeability contributes to many diseases, including acute respiratory distress syndrome, cancer and inflammation. Most past work on vascular barrier function has focused on soluble regulators, such as tumour-necrosis factor-α. Here we show that lung vascular permeability is controlled mechanically by changes in Extracellular Matrix structure. Our studies reveal that pulmonary vascular leakage can be increased by altering Extracellular Matrix compliance in vitro and by manipulating lysyl oxidase-mediated collagen crosslinking in vivo. Either decreasing or increasing Extracellular Matrix stiffness relative to normal levels disrupts junctional integrity and increases vascular leakage. Importantly, endotoxin-induced increases of vascular permeability are accompanied by concomitant increases in Extracellular Matrix rigidity and lysyl oxidase activity, which can be prevented by inhibiting lysyl oxidase activity. The identification of lysyl oxidase and the Extracellular Matrix as critical regulators of lung vascular leakage might lead to the development of new therapeutic approaches for the treatment of pulmonary oedema and other diseases caused by abnormal vascular permeability.

  • control of lung vascular permeability and endotoxin induced pulmonary oedema by changes in Extracellular Matrix mechanics
    Nature Communications, 2013
    Co-Authors: Akiko Mammoto, Tadanori Mammoto, Mathumai Kanapathipillai, Chong Wing Yung, Elisabeth Jiang, Amanda Jiang, Kristopher A Lofgren, Elaine P S Gee
    Abstract:

    Increased vascular permeability contributes to many diseases, including acute respiratory distress syndrome, cancer and inflammation. Most past work on vascular barrier function has focused on soluble regulators, such as tumour-necrosis factor-α. Here we show that lung vascular permeability is controlled mechanically by changes in Extracellular Matrix structure. Our studies reveal that pulmonary vascular leakage can be increased by altering Extracellular Matrix compliance in vitro and by manipulating lysyl oxidase-mediated collagen crosslinking in vivo. Either decreasing or increasing Extracellular Matrix stiffness relative to normal levels disrupts junctional integrity and increases vascular leakage. Importantly, endotoxin-induced increases of vascular permeability are accompanied by concomitant increases in Extracellular Matrix rigidity and lysyl oxidase activity, which can be prevented by inhibiting lysyl oxidase activity. The identification of lysyl oxidase and the Extracellular Matrix as critical regulators of lung vascular leakage might lead to the development of new therapeutic approaches for the treatment of pulmonary oedema and other diseases caused by abnormal vascular permeability. Vascular permeability is increased by inflammation and in disorders such as acute respiratory distress syndrome. Mammoto et al. show that lung vascular permeability is controlled by the stiffness of the Extracellular Matrix and identify lysyl oxidase as a regulator of vascular leakage in pulmonary oedema in mice.

Valerie M Weaver - One of the best experts on this subject based on the ideXlab platform.

  • Extracellular Matrix remodeling and stiffening modulate tumor phenotype and treatment response
    Annual Review of Cancer Biology, 2017
    Co-Authors: Jennifer L Leight, Allison P Drain, Valerie M Weaver
    Abstract:

    Solid tumors are characterized by a remodeled and stiffened Extracellular Matrix. The Extracellular Matrix is not a passive by-product of the tumor, but actively compromises tissue-specific differentiation, enhances tumor cell proliferation and survival, and fosters tumor cell invasion and migration. The tumor Extracellular Matrix also influences the behavior of the stromal cells, which through vicious, feedforward-reinforcing pathways promote tumor progression and compromise treatment efficacy. To investigate how the tumor Extracellular Matrix alters cancer phenotype and treatment, a number of three-dimensional, organotypic culture models have been developed that employ a variety of materials, including natural matrices, collagen, fibrin, and reconstituted basement membrane gels, as well as synthetic hydrogel materials such as polyacrylamide and polyethylene glycol. These models have been used to interrogate how specific microenvironmental features modify tumor and stromal cell function and to identify t...

  • the Extracellular Matrix modulates the hallmarks of cancer
    EMBO Reports, 2014
    Co-Authors: Michael W Pickup, Janna K Mouw, Valerie M Weaver
    Abstract:

    The Extracellular Matrix regulates tissue development and homeostasis, and its dysregulation contributes to neoplastic progression. The Extracellular Matrix serves not only as the scaffold upon which tissues are organized but provides critical biochemical and biomechanical cues that direct cell growth, survival, migration and differentiation and modulate vascular development and immune function. Thus, while genetic modifications in tumor cells undoubtedly initiate and drive malignancy, cancer progresses within a dynamically evolving Extracellular Matrix that modulates virtually every behavioral facet of the tumor cells and cancer-associated stromal cells. Hanahan and Weinberg defined the hallmarks of cancer to encompass key biological capabilities that are acquired and essential for the development, growth and dissemination of all human cancers. These capabilities include sustained proliferation, evasion of growth suppression, death resistance, replicative immortality, induced angiogenesis, initiation of invasion, dysregulation of cellular energetics, avoidance of immune destruction and chronic inflammation. Here, we argue that biophysical and biochemical cues from the tumor-associated Extracellular Matrix influence each of these cancer hallmarks and are therefore critical for malignancy. We suggest that the success of cancer prevention and therapy programs requires an intimate understanding of the reciprocal feedback between the evolving Extracellular Matrix, the tumor cells and its cancer-associated cellular stroma.

  • Extracellular Matrix assembly a multiscale deconstruction
    Nature Reviews Molecular Cell Biology, 2014
    Co-Authors: Janna K Mouw, Valerie M Weaver
    Abstract:

    The biochemical and biophysical properties of the Extracellular Matrix (ECM) dictate tissue-specific cell behaviour. The molecules that are associated with the ECM of each tissue, including collagens, proteoglycans, laminins and fibronectin, and the manner in which they are assembled determine the structure and the organization of the resultant ECM. The product is a specific ECM signature that is comprised of unique compositional and topographical features that both reflect and facilitate the functional requirements of the tissue.

  • the Extracellular Matrix at a glance
    Journal of Cell Science, 2010
    Co-Authors: Christian Frantz, Kathleen M Stewart, Valerie M Weaver
    Abstract:

    ![Figure][1] The Extracellular Matrix (ECM) is the non-cellular component present within all tissues and organs, and provides not only essential physical scaffolding for the cellular constituents but also initiates crucial biochemical and biomechanical cues that are required for tissue