Relevant bibliographies by topics / Extracellular matrix Physiology

Academic literature on the topic 'Extracellular matrix Physiology'

Author: Grafiati
Published: 4 June 2021
Last updated: 28 January 2023

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Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Journal articles on the topic "Extracellular matrix Physiology":

1

Roman, Jesse, Andrew H. Limper, and John A. McDonald. "Lung Extracellular Matrix: Physiology and Pathophysiology." Hospital Practice 25, no. 11 (November 15, 1990): 125–40. http://dx.doi.org/10.1080/21548331.1990.11704038.

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Bloksgaard, Maria, Merry Lindsey, and Luis A. Martinez-Lemus. "Extracellular matrix in cardiovascular pathophysiology." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 6 (December 1, 2018): H1687—H1690. http://dx.doi.org/10.1152/ajpheart.00631.2018.

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Abstract:
The extracellular matrix (ECM) actively participates in diverse aspects of cardiovascular development and physiology as well as during disease development and progression. ECM roles are determined by its physical and mechanical properties and by its capacity to both release bioactive signals and activate cell signaling pathways. The ECM serves as a storage depot for a wide variety of molecules released in response to injury or with aging. Indeed, there is a plethora of examples describing how cells react to or modify ECM stiffness, how cells initiate intracellular signaling pathways, and how cells respond to the ECM. This Perspectives article reviews the contributions of 21 articles published in the American Journal of Physiology-Heart and Circulatory Physiology in response to a Call for Papers on this topic. Here, we summarize the contributions of these studies focused on the cardiac and vascular ECM. We highlight the translational importance of these studies and conclude that the ECM is a critical component of both the heart and vasculature. Readers are urged to examine and learn from this special Call for Papers.
3

Wijsman, Pieta C., Lisa H. van Smoorenburg, Daniël M. de Bruin, Jouke T. Annema, Huib AM Kerstjens, Onno M. Mets, Maarten van den Berge, Peter I. Bonta, and Janette K. Burgess. "Imaging the pulmonary extracellular matrix." Current Opinion in Physiology 22 (August 2021): 100444. http://dx.doi.org/10.1016/j.cophys.2021.05.007.

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Rienks, Marieke, Anna-Pia Papageorgiou, Nikolaos G. Frangogiannis, and Stephane Heymans. "Myocardial Extracellular Matrix." Circulation Research 114, no. 5 (February 28, 2014): 872–88. http://dx.doi.org/10.1161/circresaha.114.302533.

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Davis, George E., and Donald R. Senger. "Endothelial Extracellular Matrix." Circulation Research 97, no. 11 (November 25, 2005): 1093–107. http://dx.doi.org/10.1161/01.res.0000191547.64391.e3.

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Tayebjee, Muzahir H., Robert J. MacFadyen, and Gregory YH Lip. "Extracellular matrix biology." Journal of Hypertension 21, no. 12 (December 2003): 2211–18. http://dx.doi.org/10.1097/00004872-200312000-00002.

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Ramirez, Francesco, Lynn Y. Sakai, Harry C. Dietz, and Daniel B. Rifkin. "Fibrillin microfibrils: multipurpose extracellular networks in organismal physiology." Physiological Genomics 19, no. 2 (October 4, 2004): 151–54. http://dx.doi.org/10.1152/physiolgenomics.00092.2004.

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Organismal physiology depends significantly on the proper assembly of extracellular matrix (ECM) macroaggregates that impart structural integrity to the connective tissue. Recent genetic studies in mice have unraveled unsuspected new functions of architectural matrix components in regulating signaling events that modulate patterning, morphogenesis, and growth of several organ systems. As a result, a new paradigm has emerged whereby tissue-specific organization of the ECM dictates not only the physical properties of the connective tissue, but also the ability of the matrix to direct a broad spectrum of cellular activities through the regulation of growth factor signaling. These observations pave the way to novel therapeutic approaches aimed at counteracting the deleterious consequences of perturbations of connective tissue homeostasis.
8

Vogel, Viola. "Unraveling the Mechanobiology of Extracellular Matrix." Annual Review of Physiology 80, no. 1 (February 10, 2018): 353–87. http://dx.doi.org/10.1146/annurev-physiol-021317-121312.

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Brown, Lindsay. "Cardiac extracellular matrix: a dynamic entity." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 3 (September 2005): H973—H974. http://dx.doi.org/10.1152/ajpheart.00443.2005.

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Ma, Zihan, Chenfeng Mao, Yiting Jia, Yi Fu, and Wei Kong. "Extracellular matrix dynamics in vascular remodeling." American Journal of Physiology-Cell Physiology 319, no. 3 (September 1, 2020): C481—C499. http://dx.doi.org/10.1152/ajpcell.00147.2020.

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Vascular remodeling is the adaptive response to various physiological and pathophysiological alterations that are closely related to aging and vascular diseases. Understanding the mechanistic regulation of vascular remodeling may be favorable for discovering potential therapeutic targets and strategies. The extracellular matrix (ECM), including matrix proteins and their degradative metalloproteases, serves as the main component of the microenvironment and exhibits dynamic changes during vascular remodeling. This process involves mainly the altered composition of matrix proteins, metalloprotease-mediated degradation, posttranslational modification of ECM proteins, and altered topographical features of the ECM. To date, adequate studies have demonstrated that ECM dynamics also play a critical role in vascular remodeling in various diseases. Here, we review these related studies, summarize how ECM dynamics control vascular remodeling, and further indicate potential diagnostic biomarkers and therapeutic targets in the ECM for corresponding vascular diseases.
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Journal articles Dissertations / Theses Books

Dissertations / Theses on the topic "Extracellular matrix Physiology":

1

Hipps, Deborah Sally. "Characterisation of gelatinase, a metalloproteinase involved in extracellular matrix degradation." Thesis, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315125.

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Al-Jamal, Rehab. "The interaction between dynamic lung physiology, the extracellular matrix and mechanical strain /." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=37861.

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Recently, various proteoglycans (PGs) have been identified in the lung. The first objective of this thesis was to test the hypothesis that matrix glycosaminoglycans contribute to lung tissue viscoelasticity. Lung parenchymal strips were exposed to specific glycosaminoglycans-degradating enzymes to determine whether the mechanical properties of the tissue were affected. The degradation of heparan sulphate and chondroitin/dermatan sulphate glycosaminoglycans caused significant increases in energy dissipation and dynamic resistance relative to control strips. Hyaluronidase treatment did not alter any of the dynamic or static measures. Since PGs were found to be part of the stress bearing structure, the second part of the thesis aimed at examining whether subjecting the lung to excessive mechanical force can cause alteration in PG composition so as to adapt to the altered stress bearing requirement. To address this hypothesis, the effect of different ventilation regimes on lung tissue mechanics and PGs was examined in an in vivo rat model. After 2 h of mechanical ventilation, lung tissue elastance and resistance were significantly increased in rats ventilated with tidal volume of 30 ml/kg at 0 positive end-expiratory pressure (Vt30PEEP0) as compared to controls (Vt8PEEP1.5). Versican, a basement membrane heparan sulphate PG and biglycan, were all increased in rat lungs ventilated with Vt30PEEP0 as compared to control. These data demonstrated that alterations in lung tissue mechanics with excessive mechanical ventilation are accompanied by changes in all classes of ECM PGs. However, whether the alteration seen in PG composition resulted from excessive mechanical ventilation directly was unclear. In addition the cellular source of these PGs was not determined. Therefore, the aim of the third part of the thesis was to investigate and characterize the effect of mechanical strain on lung fibroblast PG production in vitro. We found cell layer associated versican protein in
3

Pasternyk, Stephanie Marika 1983. "Effect of extracellular matrix and mechanical strain on airway smooth muscle." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111560.

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Airway remodeling in asthma includes alterations in extracellular matrix and airway smooth muscle (ASM) mass. For this study, ASM cells were obtained from rats that were challenged with ovalbumin (OVA) or saline (SAL) as control. OVA and SAL cells were seeded on plastic control (PC) or on plates coated with decorin or biglycan. OVA cell number was significantly increased versus SAL cells, for cells seeded on PC (48 h). A significant decrease in cell number was observed for both OVA and SAL cells seeded on decorin compared to PC cells (48 h). OVA cells, however, showed a more modest reduction in cell number. Furthermore, biglycan decreased SAL cell number only. Compared to no strain (NS), mechanical strain (S) reduced cell number for OVA and SAL cells on all matrices. In addition, S up-regulated expression of beta 1-integrin relative to NS controls. Results suggest an ability of ASM cells to be modulated by matrix and mechanical stimulation.
4

Kidd, Kameha Rae. "Angiogenesis and neovascularization in association with extracellular matrix protein modified biomaterials." Diss., The University of Arizona, 2002. http://hdl.handle.net/10150/279992.

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Synthetic biomedical implants are used to replace diseased tissues and organs. Unfortunately, these implants often fail due to a lack of biocompatibility and poor integration by the recipient. This implant failure is associated with the formation of an avascular fibrous capsule and chronic inflammatory response. Additionally, small diameter vascular grafts have complications associated with surface thrombogenenicity and intimal hyperplasia. Porous polymers are often incorporated in the construction of biomedical devices because they permit tissue integration and improved biocompatibility. While the inclusion of porosity has enhanced device performance, these devices still do not perform optimally. The incorporation of a vascular network in association with and within the pores of these materials is believed to improve tissue integration and long-term device function. Several approaches are actively being studied for their ability to stimulate new vessel growth, angiogenesis, as well as to improve the direct interaction of cells with material surfaces. The process of angiogenesis involves the coordinated involvement of both soluble and insoluble factors such as growth factors and cytokines, and extracellular matrix proteins respectively. Often, growth factors and cytokines are expressed by the inflammatory cells associated with the biomedical implants, but the microenvironment within the polymer remains unstable with respect to the presence of the appropriate extracellular matrix proteins. The overall hypothesis of this dissertation is that the reestablishment of an extracellular microenvironment on and within a porous polymer will provide the appropriate substrates for promoting angiogenesis and neovascularization of porous polymers. The results of the studies within this dissertation demonstrate that extracellular matrix modifications of commercially available expanded polytetrafluoroethylene (ePTFE) successfully promote new vessel growth in the tissue surrounding the implant, termed angiogenesis, and new vessel growth within the pores of the polymer, termed neovascularization. Furthermore, the extracellular matrix protein laminin 5 was determined to promote human microvessel endothelial cell adhesion to ePTFE as well as support angiogenesis and neovascularization when used as a surface modification of ePTFE. Based on these studies, the extracellular matrix protein, laminin 5, could be utilized in the tissue engineering of biomedical implant devices to promote increased new vessel integration and improve the long-term viability of these devices.
5

Cambell, Stephen Sean. "Morphology and histochemistry of the extracellular matrix of embryos following freeze substitution of the starfish Pisaster ochraceus." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/28938.

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All developing embryos contain an extracellular matrix (ECM) consisting of proteins, glycoproteins, and proteoglycans. These components are important for morphogenetic processes such as cell migration, cell differentiation and cell death. The ECM of the starfish, Pisaster ochraceus, consists of three major components: A hyaline layer which coats the external surface of the embryo; a basal lamina which lines the basal surfaces of the epithelia; and a blastocoelic component which fills the embryonic cavity or blastocoel. Observations of chemically fixed asteroid embryos have revealed the hyaline layer to contain five sub-layers of fibrous strands encrusted with amorphous material. Strands of a similar nature form a meshwork within the fluid-filled blastocoel. Recent studies of the living embryo, however, have suggested that the ECM within the blastocoel of echinoderms, including the asteroid, is a gel-like substance and not a fluid with extracellular fibres. Since artefacts imposed by chemicals such as aldehydes and osmium are well documented, a method of preservation, which does not involve the use of these chemicals, may resolve the apparent conflict over the nature of the ECM of the asteroid embryo. Freeze substitution, an expensive cryofixation technique which has proven successful in fixing vertebrate tissue, does not require the use of aldehydes and osmium. The initial objective of this study was to devise an inexpensive, easily employable freeze substitution technique which would allow good preservation of cellular and extracellular elements of the embryonic starfish, Pisaster ochraceus. A plunge freezing apparatus was constructed which consisted of a Dewer flask filled with liquid nitrogen, a small cup was filled with cryogen and inserted into the nitrogen, and a motor which constantly stirred the cryogen. Embryos were isolated on copper freeze-fracture grids and plunged into the cryogen. After considering four different cryogens and four separate cryoprotectants, cryoprotecting asteroid embryos with propylene glycol and plunging them into supercooled propane was found to provide optimal preservation. Frozen embryos were freeze substituted in anhydrous ethanol at -90 °C, osmicated, and embedded for ultrastructural and histochemical analysis. Following freeze substitution, the blastocoel appears to contain a gel-like substance, rich in sulfated GAG's, with extracellular fibres and not a fluid with fibres. In addition, the hyaline layer was found to consist of at least six sub-layers of greater thickness than was seen in chemically fixed embryos. Histochemical studies demonstrated that both sulfated and unsulfated GAG's were present in these layers. The morphological differences among the sub-layers suggest that some sub-layers may have unique functions while others may have functions shared by other sub-layers. Freeze substitution also revealed the presence of microvillus associated bodies, structures which may represent major attachment points of the hyaline layer to the epithelium. Although the fixation of asteroid embryos by freeze substitution is a lengthy process, taking four to five days, the resulting preservation, particular!ly of the ECM components, justifies its use over chemical fixations. Material preserved by freeze substitution can be used for histochemical studies and, since aldehydes and heavy metals are not necessary for successful preservation, may also prove useful for immunocytochemical studies.
Medicine, Faculty of
Graduate
6

Yu, Xuefeng. "Mechanism of osteoclast migration : effect of chemoattractant cytokines, extracellular matrix proteins, and proteinase inhibitors." Thesis, University of Sheffield, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287659.

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Nieves, Daniel. "Probing the structure of the extracellular matrix using gold nanoparticle based single molecule microscopy." Thesis, University of Liverpool, 2013. http://livrepository.liverpool.ac.uk/16533/.

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The observation of single biomolecules via optical microscopy eliminates all the implicit averaging of ensemble techniques and thereby provides access to the heterogeneity of molecular systems that will be the key to at least some biological functions. The implementation of photothermal microscopy at the University of Liverpool to achieve the detection of single gold nanoparticles over long times at high signal-to-noise-ratio is presented here, along with the development of Photothermal Raster Image Correlation Spectroscopy, PhRICS. PhRICS was shown to be equally effective as Photothermal Absorption Correlation Spectroscopy, PhACS, in the determination of the hydrodynamic diameter of colloidal gold nanoparticles in solution. The use of gold nanoparticles as labels for biomolecules has been of great interest due to their favorable optical properties and surface chemistry. The development of a new strategy for the covalent biofunctionalisation of gold nanoparticles with a single maleimide group is described. Nanoparticles functionalised this way were used to label FGF-2 protein and heparin-derived oligosaccharides. Both the PhRICS and the new nanoparticles developed in this thesis are combined to investigate the heterogeneity of FGF binding to heparin-derived oligosaccharides and to HS in the pericellular matrix of Rama 27 fibroblasts. The cooperativity of the interaction of FGF-2 with a dodecasaccharide is investigated. Although oligomerization of FGF-2 on the dodecasaccharide is observed, it is not cooperative. The first photothermal imaging of FGF-1 in the pericellular matrix of Rama 27 fibroblasts reveals that its diffusion is quite different from FGF-2. Imaging of FGF-2 on live cells is also revisited and probed with PhRICS. In comparison to photothermal tracking, PhRICS indicates that FGF-2 diffuses faster than first thought, and that the pericellular matrix is remodeling at timescales much shorter than previously observed.
8

Roy, Joy. "Extracellular matrix-mediated signaling in the regulation of vascular smooth muscle cell phenotype and function /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4877-1/.

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McGuire, Vincent Michael. "Assembly and function of the PsB multiprotein complex during spore differentiation in Dictyostelium discoideum /." free to MU campus, to others for purchase, 1996. http://wwwlib.umi.com/cr/mo/fullcit?p9737858.

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Saban, Melissa. "The effect of extracellular matrix on airway smooth muscle cell contractile protein expression and calcium response to serotonin." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103604.

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The asthmatic airway wall is characterized by airway remodeling, including changes in the extracellular matrix (ECM) and increased airway smooth muscle (ASM) cell mass. Further, asthmatic ASM has been shown to demonstrate enhanced contractility. Recently, we and others have shown that alterations in the matrix upon which ASM cells are grown in culture, can affect the degree of ASM cell proliferation and apoptosis. Whether changes in matrix can affect ASM cell contractility is less clear. ASM cells were isolated from the trachea of Brown Norway (BN) rats sensitized subcutaneously with ovalbumin (OVA) and challenged with either OVA or saline (SAL) as a control. Cells were grown in culture on plastic as a control, or on plates previously coated with collagen I (col), decorin (dcn) or biglycan (bgn). Contractile protein expression as well as single cell Ca2+ responses to serotonin was measured. Both SAL and OVA ASM cells grown on col had a significant reduction in α-smooth muscle actin (α-SMA) and calponin content. A significant increase in α-SMA and calponin was observed in OVA ASM cells grown on bgn but not in SAL cells. Dcn did not significantly affect α-SMA or calponin in SAL or OVA cells. Ca2+ responses to serotonin were significantly decreased in OVA cells compared to SAL cells grown on plastic, but this was not seen in cells grown on any other matrix. These experiments will help contribute to our understanding of ECM and its potential effects on mechanisms involved in smooth muscle contraction.
Les asthmatiques se caractérisent par un remodelage des voies respiratoires, incluant des changements dans la matrice extracellulaire et une augmentation de muscle lisse des voies respiratoires (MLVR). Aussi, les muscles lisses des asthmatiques ont une contractilité augmentée. Récemment on a montré qu'en changeant la matrice extracellulaire sur laquelle les muscles lisses sont cultivés, on peut affecter leur prolifération et l'apoptose. Mais on ne sait pas encore si la matrice extracellulaire peut affecter la contractilité des muscles lisses. Les muscles lisses ont été isolés des rats « Brown Norway » qui ont été sensibilisés avec l'ovalbumine (OVA) et ont été provoqués avec OVA ou saline (SAL) comme contrôle. Des cellules ont été semées sur un contrôle plastique ou sur des plats enduits de collagène (col), de décorine (dcn), ou de biglycane (bgn). Le niveau des protéines contractiles et la réponse du Ca2+ à l'ajout de serotonine dans une cellule unique a été mesuré. Les cellules OVA et SAL du MLVR qui ont été cultivées sur du col ont montré une réduction substantielle de leur contenu en α-SMA et calponine. Quand cultivées sur du bgn, une augmentation considérable du α-SMA et du calponine a été observée dans les cellules OVA du MLVR mais ceci n'a pas été observé sur des cellules SAL. Cependant quand on a semé les cellules SAL et OVA avec dcn, on n'a pas observé un effet significatif du niveau de calponine et α-SMA. La réaction du Ca2+ à la serotonine a diminué substantiellement dans les cellules OVA en comparaison à l'effet remarqué dans les cellules SAL, quand ces cellules ont été cultivées sur un contrôle plastique. Ces expériences contribuent à notre compréhension de l'importance des matrices extracellulaires dans leur contribution de l'augmentation de la contractilité du MLVR tel que décrit dans l'asthme.
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Books on the topic "Extracellular matrix Physiology":

1

Hynes, Richard O., and Kenneth M. Yamada. Extracellular matrix biology. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2012.

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Karamanos, Nikos K. Extracellular matrix: Pathobiology and signaling. Berlin: Walter de Gruyter, 2012.

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A, Zderic Stephen, ed. Muscle, matrix, and bladder function. New York: Plenum Press, 1995.

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Matrix Metalloproteinase Conference (1989 Sandestin Beach, Fla.). Matrix metalloproteinases and inhibitors: Proceedings of the Matrix Metalloproteinase Conference held at Sandestin Beach, FL, September 11-15, 1989. Edited by Birkedal-Hansen Henning. Stuttgart: G. Fischer Verlag, 1992.

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Shrestha, Prashanta. Tenascin: An extracellular matrix protein in cell growth, adhesion and cancer. New York: Chapman & Hall, 1997.

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Alta, Smit, ed. Introduction to bioregulatory medicine. Stuttgart: Thieme, 2009.

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Johnson, A. Wagoner. Mechanobiology of Cell-Cell and Cell-Matrix Interactions. Boston, MA: Springer Science+Business Media, LLC, 2011.

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International Symposium on Basement Membranes (6th 1993 Shizuoka-shi, Japan). Extracellular matrix in the kidney: 6th International Symposium on Basement Membrane, Shizuoka, May 29-June 1, 1993. Edited by Koide Hikaru and Hayashi T. Basel: Karger, 1994.

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Mueller, Margareta M. Tumor-Associated Fibroblasts and their Matrix: Tumor Stroma. Dordrecht: Springer Science+Business Media B.V., 2011.

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F, Cserr Helen, New York Academy of Sciences., and Mount Desert Island Biological Laboratory., eds. The Neuronal microenvironment. New York, N.Y: New York Academy of Sciences, 1986.

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Book chapters on the topic "Extracellular matrix Physiology":

1

Nguyen, David H. "Macrophages, Extracellular Matrix, and Estrogens in Breast Cancer Risk." In Systems Biology of Tumor Physiology, 1–19. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-25601-6_1.

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Nag, Sukriti, Dan Kilty, and Shruti Dev. "Extracellular Matrix Proteins in Cerebral Vessels in Chronic Hypertension." In Biology and Physiology of the Blood-Brain Barrier, 327–31. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-9489-2_53.

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Rajesh, Y., and Mahitosh Mandal. "Regulation of Extracellular Matrix Remodeling and Epithelial-Mesenchymal Transition by Matrix Metalloproteinases: Decisive Candidates in Tumor Progression." In Proteases in Physiology and Pathology, 159–94. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-2513-6_9.

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Kramer, M. D., R. Batrla, G. M. Hänsch, and J. Reinartz. "Plasmin-Mediated Pericellular Proteolysis by Keratinocytes: Extracellular Matrix Reorganization vs Tissue Damage." In Wound Healing and Skin Physiology, 201–11. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-77882-7_17.

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Yamamoto, Kei, Sophie Fischer-Holzhausen, Maria P. Fjeldstad, and Mary M. Maleckar. "Ordinary Differential Equation-based Modeling of Cells in Human Cartilage." In Computational Physiology, 25–39. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-05164-7_3.

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AbstractChondrocytes produce the extracellular cartilage matrix required for smooth joint mobility. As cartilage is not vascularised, and chondrocytes are not innervated by the nervous system, chondrocytes are therefore generally considered non-excitable. However, chondrocytes do express a range of ion channels, ion pumps, and receptors involved in cell homeostasis and cartilage maintenance. Dysfunction in these ion channels and pumps has been linked to degenerative disorders such as arthritis. Because the electrophysiological properties of chondrocytes are difficult to measure experimentally, mathematical modelling can instead be used to investigate the regulation of ionic currents. Such models can provide insight into the finely tuned parameters underlying fluctuations in membrane potential and cell behaviour in healthy and pathological conditions. Here, we introduce an open-source, intuitive, and extendable mathematical model of chondrocyte electrophysiology, implementing key proteins involved in regulating the membrane potential. Because of the inherent biological variability of cells and their physiological ranges of ionic concentrations, we describe a population of models that provides a robust computational representation of the biological data. This permits parameter variability in a manner mimicking biological variation, and we present a selection of parameter sets that suitably represent experimental data. Our mathematical model can be used to efficiently investigate the ionic currents underlying chondrocyte behaviour.
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Lei, Hanqin, Violetta Delgado, Emma E. Furth, Laurie G. Paavola, Felipe Vadillo-Ortega, and Jerome F. Strauss. "A Program of Cell Death and Extracellular Matrix Degradation in Fetal Membranes Prior to Labor." In Cell Death in Reproductive Physiology, 74–77. New York, NY: Springer New York, 1997. http://dx.doi.org/10.1007/978-1-4612-1944-6_7.

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Mienaltowski, Michael J., Nicole L. Gonzales, Jessica M. Beall, and Monica Y. Pechanec. "Basic Structure, Physiology, and Biochemistry of Connective Tissues and Extracellular Matrix Collagens." In Advances in Experimental Medicine and Biology, 5–43. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-80614-9_2.

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Winram, Scott B., Glen S. Tamura, and Craig E. Rubens. "In vitro systems for investigating group B streptococcal: host cell and extracellular matrix interactions." In Methods for studying the genetics, molecular biology, physiology, and pathogenesis of the streptococci, 191–201. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-017-2258-2_21.

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Mardal, Kent-André, Marie E. Rognes, Travis B. Thompson, and Lars Magnus Valnes. "Introduction." In Mathematical Modeling of the Human Brain, 1–6. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-95136-8_1.

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AbstractOur brain is our most precious yet most mysterious organ. It consists of nearly 100 billion neurons, of which typically has 10,000 connections that extend up to a meter. As such, it is an intricate web that enable us to experience the world. In addition to neurons, the brain consists of about the same number of glial cells, around 700 kilometers of blood vessels, the extracellular matrix, and is surrounded by clear water-like cerebrospinal fluid, which together all work to maintain the delicate neurons' environment in a healthy state. At the whole-organ level, this is already incredibly complex, yet this is only part of the story; at any given time, various processes are happening in the brain, such as the electrical impulses between neurons and the complex chemical signaling that helps to maintain homeostasis. Due to the innate micro-scale complexity of the brain, a natural approach, in attempting to understand the brain's physiology and function, is offered by homogenized, continuum-based modeling; here, the focus is on modeling the large-scale behavior arising from the aggregate of small-scale contributions.
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Jones, Peter Lloyd, and Lawrence S. (Lance) Prince. "The Extracellular Matrix in Development." In Fetal and Neonatal Physiology, 59–64. Elsevier, 2011. http://dx.doi.org/10.1016/b978-1-4160-3479-7.10006-0.

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Conference papers on the topic "Extracellular matrix Physiology":

1

Riley, Graham. "MMP and Matrix Degradation in Tendon." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53233.

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Tendons are often affected by chronic pain and rupture, particularly in the middle-aged and elderly, but also in the sporting and physically active younger population. Although not life threatening, these conditions (‘tendinopathy’) are major causes of morbidity, and estimated to cost tens of millions of pounds every year in lost productivity. I have previously shown that the organisation and composition of the tendon extracellular matrix (ECM) are substantially altered in tendinopathy, and that these changes may predispose to tendon pain and rupture. I have also shown that most tendinopathy is degenerative, with changes in fibroblast activity and increased ECM turnover. ECM degradation, in both normal physiology and pathology, is largely mediated by metalloproteinase enzymes: the matrix metalloproteinases (MMP) and the ‘A Disintegrin And Metalloproteinase with ThromboSpondin motifs’ (ADAMTS). I have previously shown that there are differences in MMP activity in chronic tendinopathy compared to acute tendon injuries, as well as differences in collagen turnover between tendons. Thus, although it is not known which enzymes are implicated, perturbation of the balance of metalloproteinase activities is a potential cause of tendinopathy.
2

Lee, Sheng-Lin, Ali Nekouzadeh, Kenneth M. Pryse, Elliot L. Elson, and Guy M. Genin. "Dynamics of Stretch-Induced Stress Fiber Remodeling in 3D Cell Culture." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53954.

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The responses of living cells to mechanical stimuli are believed to underlie diseases such as fibrotic cardiomyopathy [1] and asthma [2]. Emerging evidence suggests that mechanical signals transduced through the actin cytoskeleton and its connections to the extracellular matrix (ECM) have important effects on cell physiology and tissue development [13]. Understanding the responses of cells in realistic mechanical environments to mechanical stimuli is therefore of great importance to understanding development and disease.
3

Zhang, Dajun, Sheldon Weinbaum, and Stephen C. Cowin. "Electrical Signal Transmission in a Bone Cell Network: The Influence of a Discrete Gap Junction." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0288.

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Abstract Live bone is a very dynamic tissue under constant remodeling in response to the mechanical loading it sustains. However, the exact load-sensing mechanism of bone tissue is not yet clear. Recent studies suggest that the electrical aspect of bone physiology, especially the streaming potential, may play an important role in relaying the mechanical signal to the effector bone cells in bone remodeling [1] [2] [3]. In this paper, we use cable theory to calculate the intracellular potential and current in the bone cell network induced by the extracellular strain generated streaming potentials (SGPs). As an extension to our earlier paper on this subject, Zhang et al. [5], we focus our attention on the following five aspects: <1> influence of the axisymmetric, cylindrical geometry of the osteon on the SGP calculation; <2> influence of one discrete gap junction in a cellular cable; <3> influence of a range of the membrane resistance (hence the membrane time constant); <4> influence of the extracellular glycocalyx (GAG) fiber matrix in the lacunae-canaliculi space on the SGP calculation; <5> influence of a range of the membrane leakage area of a resting osteoblast as one end of the cellular cable.
4

Marshall, Lauren, Andra Frost, Tim Fee, and Joel Berry. "Assembly and Characterization of 3D, Vascularized Breast Cancer Tissue Mimics." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14199.

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Drug development platforms such as two-dimensional (2D) in vitro cell culture systems and in vivo animal studies do not accurately predict human in vivo effectiveness of candidate therapeutics [1]. Cell culture systems have limited similarities to primary human cells and tissues as only one cell type is employed and animal studies have a generally limited ability to recapitulate human drug response as different species have differences in metabolism, physiology, and behavior. Mike Leavitt, a former U.S. Secretary of Health and Human Services, has stated that “currently, nine out of ten experimental drugs fail in clinical studies because we cannot accurately predict how they will behave in people based on laboratory and animal studies” [2]. Therefore, this research project is focused on developing an in vitro platform to test candidate therapeutics for more efficacious predictions of human response. We have fabricated a three-dimensional (3D) breast cancer tissue volume containing a vascular network. This vascular network is necessary because current in vitro systems (e.g., rotating bioreactors, suspension of spheroids, and growth on a porous scaffold) are limited in size (1–2 mm) by their absence of micrometer-scale blood flow micro-channels that allow for oxygen and nutrient diffusion into the tissue [4]. The extracellular matrix scaffold has been developed to mimic the native extracellular matrix and includes relevant cell types (e.g., human breast cancer epithelial cells and human breast fibroblasts) along with the prefabricated vascular network (prevascularization). These systems are intended to support long-term growth, recapitulate physiological tissue function, and accurately model response to treatment. It is hypothesized that the development of reproducible tissue volumes will transform breast cancer drug development by providing reliable, cost-effective models that can more accurately predict therapeutic efficacy than current preclinical in vivo and in vitro models.
5

Bhatnagar, Rajendra S., Jing Jing Qian, Anna Wedrychowska, and Nancy Smith. "An Experimental Model for Investigating Mechanotransduction in Cells: Formation of 3-D Colonies and Differentiation of Cells in the Presence of a Force-Conducting Ligand." In ASME 1998 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/imece1998-0802.

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Abstract Microgravity profoundly affects the physiology of cells. The formation of 3-D arrays by cells in microgravity environments has provided novel approaches to tissue engineering. In order fully to understand the relationship between cells and their mechanical environment, it is crucial to replicate the physiological pathways involved in the transduction of mechanical energy to chemical work. Cell behavior is modulated by exogenous and biogenic mechanical forces. One of the major mechanisms that couple mechanical signals in these tissues to an intracellular apparatus for the regulation of cell behavior involves the conduction of mechanical signals via an extensive network of collagenous extracellular matrix. Specialized receptors connect cells to collagen fibers. The junction between the ECM, its receptor integrins, and the cells’ cytoskeleton plays a crucial role in cell differentiation and morphogenesis by serving as the agent for sensing the mechanical environment. We have developed an experimental model system that allows the coupling of cells to their mechanical environment through a force transducing ligand. This system has allowed us to construct 3-D colonies of cells in which cells appear to express highly differentiated function. Such systems are likely to be useful in studies on the behavior of biological systems in the microgravity environment of space.
6

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.

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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.
7

Kang, John, Robert L. Steward, YongTae Kim, Russell Schwartz, Kathleen M. Puskar, and Philip R. LeDuc. "Response of an Actin Filament Network Model Under Cyclic Stretching Through a Coarse Grained Monte Carlo Approach." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19337.

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The cytoskeleton is a dynamic system linked to the cell’s environment through sites of potential mechanical interaction such as focal adhesions, integrins, cellular junctions, and the extracellular matrix. The physiologic mechanical stimulation experienced by cells such as endothelial cells is comprised of multiple mechanical modes (e.g., stretching and shear), thus presenting a challenge to characterize their influence on cell structure.
8

Kugler, Lindsay E., Kenneth W. Ng, Christopher J. O’Conor, Gerard A. Ateshian, and Clark T. Hung. "Scaffold Properties Play a Critical Role in the Retention of Synthesized Glycosaminoglycans in Tissue Engineered Cartilage." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176558.

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Agarose has been used as a model scaffold for cartilage tissue engineering research due to its maintenance of chondrocyte phenotype, support of cartilage tissue development, and ability to transmit mechanical stimuli [1–4]. In a previous study, the temporal application of TGF-β3 for only 2 weeks resulted in explosive growth in the functional properties of tissue engineered cartilage [5]. The role of scaffolds in tissue engineering includes providing a physiologic three-dimensional environment for cells, decreased path lengths for diffusion and retention of cell elaborated matrix. In past studies by our laboratory, it was hypothesized that the scaffold properties in engineered cartilage plays a crucial role in the retention of synthesized glycosaminoglycan (GAG) molecules, a major extracellular matrix constituent of articular cartilage [6, 7]. This study focuses on testing this hypothesis using 3%, 2%, and 1% (wt/vol) agarose as scaffolds for engineered cartilage.
9

Bell, Brett J., and Sherry L. Voytik-Harbin. "Multiaxial Study of Fibroblast Biomechanics in a 3D Collagen Matrix." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206722.

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It is becoming increasingly evident, that of the signaling modalities relevant to the cell-extracellular matrix (ECM) microenvironment, the mechanical component is a very important mediator of cell behavior (reviewed in [1, 2]). Indeed, proliferation, ECM protein expression (collagen), matrix metalloproteinase (MMP) levels, migration, and stem cell differentiation, have all been shown to be affected by mechanical environmental cues [3, 4]. Although the importance of physical signaling mechanisms has been well established, the bulk of this work has yet to be translated to a more physiologic 3D microenvironment [1]. Self-assembling collagen matrices provide a biochemically, biophysically relevant 3D model of soft tissues in which biomechanical studies can be performed [5, 6]. It is with this 3D tissue model in mind, that a biaxial mechanical testing system (BMTS) was devised, built, tested, and applied to the study of cell-ECM biomechanics. The completion of this device has enabled us, to undertake a multi-scale, multidimensional study of cell-ECM mechanics. Hierarchical quantification of cell and ECM strains using digital image correlation (DIC) facilitate a more complete understanding of the mechanical response of cells to macroscopic loads and deformations. Furthermore, transfection of cells with GFP tagged actin binding protein utrophin (UTR-GFP) enables qualitative assessment of cytoskeletal deformations [7].
10

Erickson, Geoffrey R., and Farshid Guilak. "Osmotic Stress Initiates Intracellular Calcium Waves in Chondrocytes Through Extracellular Influx and the Inositol Phosphate Pathway." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0580.

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Abstract The biophysical environment of the chondrocytes plays an important role in the health, turnover, and homeostasis of articular cartilage. Under normal physiologic loading, chondrocytes are exposed to a complex and diverse array of biophysical signals, including mechanical and osmotic stresses, fluid flow, and fluid pressures [4]. Due to the charged and hydrated nature of the extracellular matrix, mechanical compression causes exudation of interstitial fluid in cartilage, which alters the osmotic environment of the chondrocytes. Confocal microscopy studies have shown that chondrocytes lose or gain volume in response to tissue compression [4] or changes in extracellular osmolarity [3]. The active process of volume recovery subsequent to osmotic shock has been shown to initiate intracellular signaling cascades [2], which may in turn alter cellular metabolism [6]. Although the mechanisms of intracellular signaling in response to osmotic stress are not fully understood, it has been hypothesized that intracellular transients and oscillations of calcium ion (Ca2+) are involved. The objective of this study was to examine the hypothesis that osmotic stress initiates a transient increase in the concentration of intracellular calcium ion ([Ca2+]i), and to determine the mechanisms of Ca2+ mobilization in isolated chondrocytes exposed to hypo- and hyper-osmotic stress.

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