Relevant bibliographies by topics / Mechanostimulation

Academic literature on the topic 'Mechanostimulation'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Mechanostimulation"

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Govoni, Marco, Claudio Muscari, Carlo Guarnieri, and Emanuele Giordano. "Mechanostimulation Protocols for Cardiac Tissue Engineering." BioMed Research International 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/918640.

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Owing to the inability of self-replacement by a damaged myocardium, alternative strategies to heart transplantation have been explored within the last decades and cardiac tissue engineering/regenerative medicine is among the present challenges in biomedical research. Hopefully, several studies witness the constant extension of the toolbox available to engineer a fully functional, contractile, and robust cardiac tissue using different combinations of cells, template bioscaffolds, and biophysical stimuli obtained by the use of specific bioreactors. Mechanical forces influence the growth and shape of every tissue in our body generating changes in intracellular biochemistry and gene expression. That is why bioreactors play a central role in the task of regenerating a complex tissue such as the myocardium. In the last fifteen years a large number of dynamic culture devices have been developed and many results have been collected. The aim of this brief review is to resume in a single streamlined paper the state of the art in this field.
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Kadem, Laith F., K. Grace Suana, Michelle Holz, Wei Wang, Hannes Westerhaus, Rainer Herges, and Christine Selhuber-Unkel. "High-Frequency Mechanostimulation of Cell Adhesion." Angewandte Chemie International Edition 56, no. 1 (November 30, 2016): 225–29. http://dx.doi.org/10.1002/anie.201609483.

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Kadem, Laith F., K. Grace Suana, Michelle Holz, Wei Wang, Hannes Westerhaus, Rainer Herges, and Christine Selhuber-Unkel. "High-Frequency Mechanostimulation of Cell Adhesion." Angewandte Chemie 129, no. 1 (November 30, 2016): 231–35. http://dx.doi.org/10.1002/ange.201609483.

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Ghosh, Ritesh, Adelin Barbacci, and Nathalie Leblanc-Fournier. "Mechanostimulation: a promising alternative for sustainable agriculture practices." Journal of Experimental Botany 72, no. 8 (January 29, 2021): 2877–88. http://dx.doi.org/10.1093/jxb/erab036.

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Abstract Plants memorize events associated with environmental fluctuations. The integration of environmental signals into molecular memory allows plants to cope with future stressors more efficiently—a phenomenon that is known as ‘priming’. Primed plants are more resilient to environmental stresses than non-primed plants, as they are capable of triggering more robust and faster defence responses. Interestingly, exposure to various forms of mechanical stimuli (e.g. touch, wind, or sound vibration) enhances plants’ basal defence responses and stress tolerance. Thus, mechanostimulation appears to be a potential priming method and a promising alternative to chemical-based priming for sustainable agriculture. According to the currently available method, mechanical treatment needs to be repeated over a month to alter plant growth and defence responses. Such a long treatment protocol restricts its applicability to fast-growing crops. To optimize the protocol for a broad range of crops, we need to understand the molecular mechanisms behind plant mechanoresponses, which are complex and depend on the frequency, intervals, and duration of the mechanical treatment. In this review, we synthesize the molecular underpinnings of plant mechanoperception and signal transduction to gain a mechanistic understanding of the process of mechanostimulated priming.
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Hernandez, Marylens, Julia Patzig, Sonia R. Mayoral, Kevin D. Costa, Jonah R. Chan, and Patrizia Casaccia. "Mechanostimulation Promotes Nuclear and Epigenetic Changes in Oligodendrocytes." Journal of Neuroscience 36, no. 3 (January 20, 2016): 806–13. http://dx.doi.org/10.1523/jneurosci.2873-15.2016.

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Osborn, Eric A., Aleksandr Rabodzey, C. Forbes Dewey, and John H. Hartwig. "Endothelial actin cytoskeleton remodeling during mechanostimulation with fluid shear stress." American Journal of Physiology-Cell Physiology 290, no. 2 (February 2006): C444—C452. http://dx.doi.org/10.1152/ajpcell.00218.2005.

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Fluid shear stress stimulation induces endothelial cells to elongate and align in the direction of applied flow. Using the complementary techniques of photoactivation of fluorescence and fluorescence recovery after photobleaching, we have characterized endothelial actin cytoskeleton dynamics during the alignment process in response to steady laminar fluid flow and have correlated these results to motility. Alignment requires 24 h of exposure to fluid flow, but the cells respond within minutes to flow and diminish their movement by 50%. Although movement slows, the actin filament turnover rate increases threefold and the percentage of total actin in the polymerized state decreases by 34%, accelerating actin filament remodeling in individual cells within a confluent endothelial monolayer subjected to flow to levels used by dispersed nonconfluent cells under static conditions for rapid movement. Temporally, the rapid decrease in filamentous actin shortly after flow stimulation is preceded by an increase in actin filament turnover, revealing that the earliest phase of the actin cytoskeletal response to shear stress is net cytoskeletal depolymerization. However, unlike static cells, in which cell motility correlates positively with the rate of filament turnover and negatively with the amount polymerized actin, the decoupling of enhanced motility from enhanced actin dynamics after shear stress stimulation supports the notion that actin remodeling under these conditions favors cytoskeletal remodeling for shape change over locomotion. Hours later, motility returned to pre-shear stress levels but actin remodeling remained highly dynamic in many cells after alignment, suggesting continual cell shape optimization. We conclude that shear stress initiates a cytoplasmic actin-remodeling response that is used for endothelial cell shape change instead of bulk cell translocation.
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Halbwirth, Florian, Eugenia Niculescu-Morzsa, Hannes Zwickl, Christoph Bauer, and Stefan Nehrer. "Mechanostimulation changes the catabolic phenotype of human dedifferentiated osteoarthritic chondrocytes." Knee Surgery, Sports Traumatology, Arthroscopy 23, no. 1 (November 7, 2014): 104–11. http://dx.doi.org/10.1007/s00167-014-3412-8.

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Indra, Indrajyoti, Alexander N. Gasparski, and Karen A. Beningo. "An in vitro correlation of metastatic capacity and dual mechanostimulation." PLOS ONE 13, no. 11 (November 14, 2018): e0207490. http://dx.doi.org/10.1371/journal.pone.0207490.

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John, Susan P., and Karl H. Hasenstein. "Effects of mechanostimulation on gravitropism and signal persistence in flax roots." Plant Signaling & Behavior 6, no. 9 (September 2011): 1365–70. http://dx.doi.org/10.4161/psb.6.9.16601.

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Tretner, C., U. Huth, and B. Hause. "Mechanostimulation of Medicago truncatula leads to enhanced levels of jasmonic acid." Journal of Experimental Botany 59, no. 10 (July 1, 2008): 2847–56. http://dx.doi.org/10.1093/jxb/ern145.

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Dissertations / Theses on the topic "Mechanostimulation"

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Riaz, Anjum. "Adhesion Dependent Signals : Cell Survival, Receptor Crosstalk and Mechanostimulation." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-195712.

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The integrin family of cell surface receptors is evolutionary conserved and found in all multicellular animals. In humans 8-alpha and 18-beta integrins are non-covalently associated into 24 dimers. Integrins mediate cell-extracellular matrix and cell-cell interactions and participate in cell signalling. This ideally places integrins to regulate vital processes such as cell adhesion, migration, differentiation and cytoskeleton dynamics. Integrins also play a fundamental role in regulating cell survival and anoikis. In this thesis molecular mechanisms employed by integrins to induce signal transduction, independently or through crosstalk with other receptors, were characterised. Rictor-mTOR (mTORC2) was required for Akt Ser473 phosphorylation in response to β1 integrin-mediated adhesion as well as EGF-, PDGF- or LPA-stimulation of MCF7 cells. ILK and PAK were dispensable for Akt Ser473 phosphorylation upon β1 integrin-engagement or EGF-stimulation. PAK was needed when this phosphorylation was induced by PDGF or LPA. β1 integrin-promoted cell survival during serum starvation conditions was mTORC2 dependent, indicating the importance of Akt Ser473 phosphorylation. mTORC2 was also required for Akt Ser473 phosphorylation induced upon heparanase treatment of cells. Heparanase preferred PI3K catalytic subunit p110α for the upstream lipid phosphorylation required for Akt activation. Interaction between this subunit and Ras was needed for optimal Akt phosphorylation upon heparanase exposure. Cell adhesion strongly promoted heparanase signalling, which was more efficient in β1 integrin-expressing fibroblasts compared to cells lacking this subunit. The cooperative signalling between integrins and heparanase involved FAK and PYK2 since simultaneous silencing of these kinases suppressed heparanase-triggered Akt activation. Furthermore, the resistance of cells to apoptosis induced by H2O2 or serum starvation was promoted by heparanase.  Integrin stimulation by adhesion or cyclic stretching showed divergent downstream signalling responses. Cell attachment on integrin-specific ligands lead to robust phosphorylation of several intracellular integrin-effectors, e.g. p130CAS, FAK, Akt and ERK 1/2. However, mechanical cell stretching only triggered prominent phosphorylation of ERK 1/2. Signalling induced at early stages of integrin-mediated cell adhesion occurred independently of intracellular contraction. Reactive oxygen species (ROS) generated during adhesion and cell stretching influenced integrin signalling. Inhibition of mitochondrial ROS production blocked adhesion-induced Akt phosphorylation. In contrast, stretch-induced ERK 1/2 phosphorylation was elevated when extracellular ROS was scavenged. These results indicate that the two types of integrin stimuli generate signals by different mechanisms.
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Norman, Harrison E. "A device for the graded mechanostimulation of cultured neurons." Thesis, Georgia Institute of Technology, 2014. http://hdl.handle.net/1853/53105.

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This work presents an in vitro platform for studying the effects of physiologically relevant, axonally applied mechanical insult to neurons in culture. Design considerations are presented, and finite element studies are shown to establish proof of concept. The mold for creating the device was microfabricated in a cleanroom for use in the replica molding of the device. The process of fabricating the final device is then detailed. Initial biocompatibility assays are presented, and experiments for characterizing the function of the device are proposed.
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Hayward, Mary-Kate. "Mechanostimulation of integrin αvβ6 and fibronectin in DCIS myoepithelial cells." Thesis, Queen Mary, University of London, 2018. http://qmro.qmul.ac.uk/xmlui/handle/123456789/54057.

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Alterations to the tumour microenvironment is a common feature of many cancers, including breast cancer, and there is increasing evidence that alterations to the microenvironment, including; increased integrin expression, ECM deposition and protease activity, promote cancer progression. Most invasive breast cancers arise from a preinvasive stage, ductal carcinoma in situ (DCIS). Previous work in our laboratory has shown the microenvironment of DCIS is altered, such that myoepithelial cells (MECs) switch to a tumour-promoting phenotype, associated with upregulation of integrin αvβ6 and fibronectin (FN) expression. Mechanisms by which integrin αvβ6 and FN expression are regulated is unclear. We show DCIS progression into invasion is accompanied by an increase in MEC expression of integrin αvβ6 and periductal FN deposition, and their expression were associated in DCIS. These findings were modelled in isolated primary DCIS-MECs, primary normal MECs and MEC lines, with and without integrin αvβ6 expression, where integrin αvβ6-positive MECs upregulating FN expression. We identified integrin αvβ6-positive DCIS ducts were larger than integrin αvβ6-negative DCIS ducts, and mechanical stretching of primary normal MECs and a normal MEC line led to upregulation of integrin αvβ6 expression and FN deposition in a TGFβ-dependent manner. We further show upregulation of integrin αvβ6 and FN by MECs mediate TGFβ-dependent upregulation of MMP13 which promotes breast cancer cell invasion in vitro. These data show altered tissue mechanics in DCIS and MEC expression of integrin αvβ6 and FN deposition are linked, and implicate TGFβ in their activation. These findings suggest integrin αvβ6 and FN may be used as markers to stratify DCIS patients.
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Book chapters on the topic "Mechanostimulation"

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Schumann, Stefan, Katharina Gamerdinger, Caroline Armbruster, Constanze Dassow, David Schwenninger, and Josef Guttmann. "Mechanostimulation and Mechanics Analysis of Lung Cells, Lung Tissue and the Entire Lung Organ." In Notes on Numerical Fluid Mechanics and Multidisciplinary Design, 129–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-20326-8_8.

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"Mechanostimulation in Bone and Tendon Tissue Engineering." In Mechanobiology Handbook, 435–58. CRC Press, 2011. http://dx.doi.org/10.1201/b10780-25.

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Conference papers on the topic "Mechanostimulation"

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Gurkan, Umut Atakan, Alexandra Dubikovsky, Lynetta J. Freeman, Paul W. Snyder, Russell D. Meldrum, and Ozan Akkus. "In Vivo Actuation System for Mechanostimulation of Large Wound Healing." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53183.

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The incidence of large open wounds in the US is estimated to be about 5–7 million per year which results in a cost of greater than $20 billion for wound management [1]. Large open wounds occur due to burns, trauma, and secondary to surgical interventions, ulcers or pressure sores. The current clinical practice is to treat large open wounds by delayed primary closure where skin is stretched under constant tension to approximate wound edges by relying on the extensibility of the neighboring skin, by skin grafting or by managing the wound to heal by second intention. Delayed primary closure is inapplicable when the strength of the skin is compromised (e.g. age, diabetes). Furthermore, delayed primary closure usually leads to excessive wound tension which introduces hypertrophic scars [2] and ischemia [3] to the skin and the underlying muscles. Skin autografts may result in morbidity of the donor site. Therefore, there is the need for noninvasive methods which will enable large wound closure in a reasonable time frame with minimal scar formation while alleviating or reducing the need for skin graft harvest.
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Junkin, Michael, Yi Lu, Juexuan Long, Pierre A. Deymier, James B. Hoying, and Pak Kin Wong. "A mechanostimulation system for revealing intercellular calcium communication in HUVEC networks." In 2012 IEEE 6th International Conference on Nano/Molecular Medicine and Engnieering (NANOMED). IEEE, 2012. http://dx.doi.org/10.1109/nanomed.2012.6509116.

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Junkin, M., Y. Lu, P. Deymier, and P. K. Wong. "An integrated mechanostimulation system for probing architecture based calcium signaling in HUVEC cells." In 2011 IEEE 24th International Conference on Micro Electro Mechanical Systems (MEMS). IEEE, 2011. http://dx.doi.org/10.1109/memsys.2011.5734569.

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Lorusso, D., H. N. Nikolov, T. Chmiel, R. J. Beach, S. M. Sims, S. J. Dixon, and D. W. Holdsworth. "A device for real-time live-cell microscopy during dynamic dual-modal mechanostimulation." In SPIE Medical Imaging, edited by Andrzej Krol and Barjor Gimi. SPIE, 2017. http://dx.doi.org/10.1117/12.2253904.

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