Relevant bibliographies by topics / Mechanotransduction

Academic literature on the topic 'Mechanotransduction'

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Published: 4 June 2021
Last updated: 7 July 2024

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Journal articles on the topic "Mechanotransduction"

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French, A. S. "Mechanotransduction." Annual Review of Physiology 54, no. 1 (October 1992): 135–52. http://dx.doi.org/10.1146/annurev.ph.54.030192.001031.

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Qin, Yi-Xian, and Minyi Hu. "Mechanotransduction in Musculoskeletal Tissue Regeneration: Effects of Fluid Flow, Loading, and Cellular-Molecular Pathways." BioMed Research International 2014 (2014): 1–12. http://dx.doi.org/10.1155/2014/863421.

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While mechanotransductive signal is proven essential for tissue regeneration, it is critical to determine specific cellular responses to such mechanical signals and the underlying mechanism. Dynamic fluid flow induced by mechanical loading has been shown to have the potential to regulate bone adaptation and mitigate bone loss. Mechanotransduction pathways are of great interests in elucidating how mechanical signals produce such observed effects, including reduced bone loss, increased bone formation, and osteogenic cell differentiation. The objective of this review is to develop a molecular understanding of the mechanotransduction processes in tissue regeneration, which may provide new insights into bone physiology. We discussed the potential for mechanical loading to induce dynamic bone fluid flow, regulation of bone adaptation, and optimization of stimulation parameters in various loading regimens. The potential for mechanical loading to regulate microcirculation is also discussed. Particularly, attention is allotted to the potential cellular and molecular pathways in response to loading, including osteocytes associated with Wnt signaling, elevation of marrow stem cells, and suppression of adipotic cells, as well as the roles of LRP5 and microRNA. These data and discussions highlight the complex yet highly coordinated process of mechanotransduction in bone tissue regeneration.
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Luis Alonso, José, and Wolfgang H. Goldmann. "Cellular mechanotransduction." AIMS Biophysics 3, no. 1 (2016): 50–62. http://dx.doi.org/10.3934/biophy.2016.1.50.

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Chalfie, Martin. "Neurosensory mechanotransduction." Nature Reviews Molecular Cell Biology 10, no. 1 (January 2009): 44–52. http://dx.doi.org/10.1038/nrm2595.

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Hansen, Caroline E., Yongzhi Qiu, Owen J. T. McCarty, and Wilbur A. Lam. "Platelet Mechanotransduction." Annual Review of Biomedical Engineering 20, no. 1 (June 4, 2018): 253–75. http://dx.doi.org/10.1146/annurev-bioeng-062117-121215.

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The vasculature is a dynamic environment in which blood platelets constantly survey the endothelium for sites of vessel damage. The formation of a mechanically coherent hemostatic plug to prevent blood loss relies on a coordinated series of ligand–receptor interactions governing the recruitment, activation, and aggregation of platelets. The physical biology of each step is distinct in that the recruitment of platelets depends on the mechanosensing of the platelet receptor glycoprotein Ib for the adhesive protein von Willebrand factor, whereas platelet activation and aggregation are responsive to the mechanical forces sensed at adhesive junctions between platelets and at the platelet–matrix interface. Herein we take a biophysical perspective to discuss the current understanding of platelet mechanotransduction as well as the measurement techniques used to quantify the physical biology of platelets in the context of thrombus formation under flow.
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Persat, Alexandre. "Bacterial mechanotransduction." Current Opinion in Microbiology 36 (April 2017): 1–6. http://dx.doi.org/10.1016/j.mib.2016.12.002.

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Leckband, Deborah. "Intercellular Mechanotransduction." Biophysical Journal 114, no. 3 (February 2018): 555a. http://dx.doi.org/10.1016/j.bpj.2017.11.3033.

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Stewart, Sarah, Alastair Darwood, Spyros Masouros, Claire Higgins, and Arul Ramasamy. "Mechanotransduction in osteogenesis." Bone & Joint Research 9, no. 1 (January 2020): 1–14. http://dx.doi.org/10.1302/2046-3758.91.bjr-2019-0043.r2.

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Bone is one of the most highly adaptive tissues in the body, possessing the capability to alter its morphology and function in response to stimuli in its surrounding environment. The ability of bone to sense and convert external mechanical stimuli into a biochemical response, which ultimately alters the phenotype and function of the cell, is described as mechanotransduction. This review aims to describe the fundamental physiology and biomechanisms that occur to induce osteogenic adaptation of a cell following application of a physical stimulus. Considerable developments have been made in recent years in our understanding of how cells orchestrate this complex interplay of processes, and have become the focus of research in osteogenesis. We will discuss current areas of preclinical and clinical research exploring the harnessing of mechanotransductive properties of cells and applying them therapeutically, both in the context of fracture healing and de novo bone formation in situations such as nonunion. Cite this article: Bone Joint Res 2019;9(1):1–14.
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Uray, Iván P., and Karen Uray. "Mechanotransduction at the Plasma Membrane-Cytoskeleton Interface." International Journal of Molecular Sciences 22, no. 21 (October 26, 2021): 11566. http://dx.doi.org/10.3390/ijms222111566.

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Mechanical cues are crucial for survival, adaptation, and normal homeostasis in virtually every cell type. The transduction of mechanical messages into intracellular biochemical messages is termed mechanotransduction. While significant advances in biochemical signaling have been made in the last few decades, the role of mechanotransduction in physiological and pathological processes has been largely overlooked until recently. In this review, the role of interactions between the cytoskeleton and cell-cell/cell-matrix adhesions in transducing mechanical signals is discussed. In addition, mechanosensors that reside in the cell membrane and the transduction of mechanical signals to the nucleus are discussed. Finally, we describe two examples in which mechanotransduction plays a significant role in normal physiology and disease development. The first example is the role of mechanotransduction in the proliferation and metastasis of cancerous cells. In this system, the role of mechanotransduction in cellular processes, including proliferation, differentiation, and motility, is described. In the second example, the role of mechanotransduction in a mechanically active organ, the gastrointestinal tract, is described. In the gut, mechanotransduction contributes to normal physiology and the development of motility disorders.
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Sun, Zhiqi, Shengzhen S. Guo, and Reinhard Fässler. "Integrin-mediated mechanotransduction." Journal of Cell Biology 215, no. 4 (November 8, 2016): 445–56. http://dx.doi.org/10.1083/jcb.201609037.

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Cells can detect and react to the biophysical properties of the extracellular environment through integrin-based adhesion sites and adapt to the extracellular milieu in a process called mechanotransduction. At these adhesion sites, integrins connect the extracellular matrix (ECM) with the F-actin cytoskeleton and transduce mechanical forces generated by the actin retrograde flow and myosin II to the ECM through mechanosensitive focal adhesion proteins that are collectively termed the “molecular clutch.” The transmission of forces across integrin-based adhesions establishes a mechanical reciprocity between the viscoelasticity of the ECM and the cellular tension. During mechanotransduction, force allosterically alters the functions of mechanosensitive proteins within adhesions to elicit biochemical signals that regulate both rapid responses in cellular mechanics and long-term changes in gene expression. Integrin-mediated mechanotransduction plays important roles in development and tissue homeostasis, and its dysregulation is often associated with diseases.
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Dissertations / Theses on the topic "Mechanotransduction"

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Huang, Wei. "Polycystin-1 and Bone Mechanotransduction." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10279.

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Bone mechanotransduction is a fundamental process underlying the remarkable ability of bones to perceive surrounding physical cues and adapt their mass, structure and overall strength to their mechanical environment. Therefore, it is central to many aspects of bone biology and disease. The key to a mechanistic understanding of this process lies in better knowledge of critical signaling molecules that relay the mechanical information inside bone cells. In this thesis, we investigate the role of polycystin-1 (PC1), a proposed fluid flow sensor in kidney epithelial cells, in transducing mechanical signals in bone cells. Loss of PC1 in osteoblast lineage cells using osterix-Cre (Osx-Cre) causes mild osteopenia in mice with reduced calvarial and trabecular bone formation, and markedly attenuated anabolic bone formation responses to in vivo mechanical loading of long bones. Loss of PC1 in limb bud mesenchymal cells at an early stage causes mildly increased bone formation and a tendency to exhibit enhanced anabolic responses to in vivo mechanical loading of long bones. These findings suggest that PC1 has a complex role in different bone cell populations both during development and in bone mechanotransduction. PC1 has been shown to mediate tensile force-induced proliferation in osteoprogenitor cells (OPCs) in craniofacial sutures. To investigate the role of PC1 in periosteal osteoprogenitor mechanotransduction, we establish a shockwave-induced periosteum mechanical stress model. Shockwave treatment triggers dramatically increased cell proliferation, potent osteogenic activity, and intramembranous new bone formation in the periosteum. We show that loss of PC1 in periosteal cells (Prx1-Cre) does not affect periosteal mechanoresponsiveness to shockwave mechanical stress. These findings suggest that the role of PC1 in OPCs is likely tissue or force dependent. Fluid shear stress (FSS) in the lacunar-canalicular network is a major force element that osteocytes experience and respond to in vivo. To study the role of PC1 in FSS-mediated osteocyte/osteoblast mechanotransduction, we establish a laminar FSS system with custom-made flow chambers and a PC1-deficient osteoblast cell line. Our data show that PC1 is essential for regulation of FSS-induced initial \(Ca^{2+}\) influx in osteoblasts and mediates osteoblast FSS responses in a COX-2 and AP-1 independent manner.
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Chronopoulos, Antonios. "Mechanotransduction in health and disease." Thesis, Imperial College London, 2017. http://hdl.handle.net/10044/1/56622.

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Physical forces regulate cellular behaviour and function during all stages of life. Mechanotransduction, the process by which cells convert mechanical stimuli into biochemical signalling events is central to a number of physiological and pathological processes. The first part of this work focuses on the effect of retinoid therapy on the mechanobiology of pancreatic cancer. Pancreatic cancer is characterised by a persistent activation of stromal fibroblasts, known as pancreatic stellate cells (PSCs), which can perturb the biomechanical homeostasis of the tumour microenvironment to favour tumour invasion. Using biophysical and biological techniques, we report that all-trans retinoic acid (ATRA), an active vitamin A metabolite restores mechanical quiescence in PSCs via a mechanism involving a retinoic acid receptor beta (RAR-β)-mediated downregulation of actomyosin (MLC-2) contracility. We show that ATRA reduces the ability of PSCs to generate high traction forces and adapt to extracellular mechanical cues (mechanosensing), as well as suppresses force-mediated extracellular matrix remodelling to inhibit local cancer cell invasion in 3D organotypic models. We thus suggest that ATRA may serve as a stroma reprogramming agent for the treatment of pancreatic cancer. In the second part of this work, we focus on syndecan-4 (Syn-4) - a ubiquitous transmembrane proteoglycan receptor. We identify Syn-4 as a cellular mechanotransducer that tunes cell mechanics by eliciting a global mechanosignalling response. We outline a mechanotransduction model whereby localised tension on Syn-4 triggers a synergistic cell-wide activation of β1 integrins, in a PI3K-dependent manner, to subsequently activate the RhoA pathway and induce adaptive cell stiffening. Furthermore, syndecan-4 mediated mechanosensing is required for YAP activation and downstream changes in gene expression. We propose that this newly identified mechanotransductive ability of Syn-4 should have direct implications for the field of mechanobiology.
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Pucker, Andrew David. "Mechanotransduction in the Ciliary Muscle." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1460647729.

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Malone, Amanda Michelle Dolphin. "Mechanotransduction mechanisms in bone cells /." May be available electronically:, 2007. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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Kuck, Jan L. "Mechanotransduction in red blood cells." Thesis, Griffith University, 2023. http://hdl.handle.net/10072/421118.

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Red blood cells (RBC), the oxygen-carriers within blood, eject their nuclei and other organelles to optimise cellular mechanics for gas exchange in capillary networks. Lack of organelles, however, strictly limits circulatory longevity of these cells, due to the inability to repair damaged cellular components. Given the turnover of RBC, the cell population within blood is inherently heterogenous, comprising RBC across the whole spectrum of in vivo age. Moreover, surrender of translational capacity restricts cellular signalling within RBC to modifications of existing proteins and/or flux of ions through membrane-embedded channels, rather than alterations in protein expression. The traversal of the cardiovascular system for the purpose of gas exchange exposes RBC to varying mechanical forces. Exposure to mechanical force physically deforms the RBC membrane, which, upon cessation of force exposure, readopts its native bi-concave disc chape. Novel observations support that these mechanical forces also activate biochemical pathways that may acutely and transiently alter RBC mechanics. The molecular machinery facilitating these mechanotransduction processes in RBC, however, is largely undescribed. The aim of the present body of work was thus to elucidate i. mechanotransductive pathways in mature, enucleated RBC; ii. the contribution of mechanically-activated signalling to the regulation of RBC mechanics; and iii. the impact of sub-populations of RBC with abnormal mechanical properties on blood fluid behaviour. The salient findings of the present dissertation support the presence of a relevant post-translational signalling network in circulating, enucleated RBC, some of which is sensitive to activation by mechanical forces. The cation channel Piezo1 appears to be a central mechanism of ‘force sensing’ in these cells. That is, opening of Piezo1 in response to mechanical force facilitates influx of calciumions, which regulate RBC mechanics via diverse mechanisms, including acute shifts in cell volume, selective removal of susceptible cells within a given RBC population, and initiation of nitric oxide production. Collectively, the herein presented results enhance the current understanding of fundamental RBC physiology by elucidating hitherto unrecognised signalling pathways. Given the demonstrated relevance of these processes to the regulation of RBC mechanical properties, which determine blood fluid properties and effective gas exchange, components of mechanically-activated signalling in these cells may provide novel therapeutic targets. Moreover, adverse complications arising in scenarios where blood is exposed to mechanical forces far exceeding those investigated here, for example during transit of mechanical circulatory support devices or dialysis machines, may be linked to overactivation of mechanically-sensitive signalling.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Health Sci & Soc Wrk
Griffith Health
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Bays, Jennifer McQuown. "Mechanisms of E-cadherin mechanotransduction." Diss., University of Iowa, 2017. https://ir.uiowa.edu/etd/5711.

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Cells experience force throughout their lifetimes. Cells sense force via adhesion receptors, such as the cadherins, which anchor cells to neighboring cells, and integrins, which tether cells to the underlying matrix. Both adhesion receptors respond to force by activating signaling pathways inside the cell. These pathways trigger growth of adhesion complexes and reinforcement of the cytoskeleton in order to resist the force. These activities are energetically costly. Thus, mechanisms are needed to couple force transmission and energy production. In this thesis, I demonstrated force on cadherins activates a master regulator of energy homeostasis known as AMP-activated kinase (AMPK). In response to force, AMPK was recruited to the cadherins. AMPK promoted growth of the adhesion complex and cytoskeletal reinforcement by stimulating energy production in the cell. Additionally, AMPK formed a complex with vinculin—a protein that is recruited to both cadherins and integrins. I observed AMPK activation of vinculin dictates whether vinculin joins the cadherin complex. Conversely, AMPK activation has no bearing on vinculin recruitment to integrins. This work provides three novel contributions: (1) the first link between energy production and force transmission, (2) a molecular mechanism for how AMPK increases adhesion complex growth, and (3) an explanation for how vinculin discriminates between cadherins and integrins.
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Bouclet, Adrien. "Evolutionary implication of mechanotransduction in development." Phd thesis, Université René Descartes - Paris V, 2014. http://tel.archives-ouvertes.fr/tel-01071238.

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In this thesis, I first focused on the testing of the hypothesis of the mechanotransductive activation of the apical accumulation of Myosin-II (Myo-II) that leads to Drosophila embryos mesoderm invagination, in response to the active cell apex pulsations preceding gastrulation in the mesoderm. This hypothesis was proposed on the basis of previous experiments realized in my host lab, having consisted in the rescue of mesoderm invagination in pulsation and invagination defective mutants, in response to a simple mechanical indent of the mesoderm. Here I demonstrated quantitatively the plausibility of such mechanical trigger of the active apical accumulation of Myo-II leading to subsequent mesoderm invagination, in response to the mechanical strains developed by the endogenous pulsative movements of mesoderm cell apexes, in silico. In a second part, I tested experimentally the role of the mechanical strains developed by the very first morphogenetic movements of zebrafish (Danio rerio) and Drosophila embryos, in the early specification of mesoderm cells identity. Specifically, to test this hypothesis, I developed magnetic biophysical tools to mimic the epiboly morphogenetic movements in epiboly defective zebrafish embryos. We found the beta-catenin (B-cat) Y667 phosphorylation as the common mechano-transductive pathway involved in earliest mesoderm genes expression notail and twist respectively, in response to the very first morphogenetic movements of embryogenesis in both species, epiboly and mesoderm invagination, respectively. This allowed to suggest such mechanotransduction pathway as conserved from the last common ancestor of both species, namely the last common ancestor of bilaterians, therefore possibly involved in the origins of mesoderm emergence in the ancestor, which represents a currently important opened question of evo-devo. In a third part, I developed experiments of mechanical indent of Drosophila embryos germ cells, and demonstrated the production of generational heritable developmental defects induced on at least 3 generations. These experiments suggest accidental mechanical perturbation of germ cells as a putative new motor mode of heritable modulations in the genetic developmental program of embryogenesis, with the molecular mechanism underlying such transmission being currently in progress.
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Aragona, Mariaceleste. "Role of YAP/TAZ in Mechanotransduction." Doctoral thesis, Università degli studi di Padova, 2012. http://hdl.handle.net/11577/3422159.

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Cells perceive their microenvironment not only through soluble signals but also in term of physical and mechanical cues, such as extracellular matrix (ECM) stiffness or confined adhesiveness. By mechanotransduction systems, cells translate these stimuli into biochemical signals controlling multiple aspects of cell behavior, including growth, differentiation and cancer malignant progression; but how rigidity mechanosensing is ultimately linked to activity of nuclear transcription factors remains poorly understood. Here we report the identification of the Yorkie-homologues YAP and TAZ as nuclear relays of mechanical signals exerted by ECM rigidity and cell-shape. This regulation requires Rho activity and tension of the acto-myosin cytoskeleton but is independent from the Hippo/LATS cascade. Crucially, YAP/TAZ are functionally required for differentiation of mesenchymal stem cells induced by ECM stiffness and for survival of endothelial cells regulated by cell geometry; conversely, expression of activated YAP overrules physical constraints in dictating cell behavior. These findings identify YAP/TAZ as sensors and mediators of mechanical cues instructed by the cellular microenvironment.
Le cellule percepiscono il loro microambiente non solo attraverso molecole segnale e fattori solubili ma anche attraverso stimoli fisici e meccanici. Le cellule traducono questi stimoli in segnali biochimici attraverso un processo definito meccanotrasduzione, in grado di regolare numerosi aspetti del comportamento cellulare, tra cui crescita, differenziamento e progressione tumorale. Tuttavia, non è ancora noto come la percezione dei segnali meccanici si traduca nell’attivazione di specifici fattori di trascrizione a livello nucleare. Questo lavoro individua YAP (Yes-associated protein), e TAZ (transcriptional coactivator with PDZ-binding motif, anche noto come WWTR1), omologhi di Yorkie in Drosophila, quali fattori di trascrizione in grado di rispondere ai segnali meccanici generati dalla rigidità della matrice extracellulare e dalla forma propria di ogni singola cellula. Questa regolazione richiede l’attivazione della GTPase Rho e la presenza di un citoscheletro di actina contrattile, ma è indipendente dall’attività della via di segnale delle chinasi Hippo e LATS. Non solo YAP/TAZ vengono regolati da segnali meccanici, ma sono anche funzionalmente richiesti per il differenziamento delle cellule staminali mesenchimali indotto dalla stiffness (elasticità o rigidità) della matrice e per la sopravvivenza delle cellule endoteliali regolata dalla geometria cellulare. In maniera complementare, l’espressione di una forma attivata di YAP domina sull’azione degli stimoli fisici nel determinare il destino cellulare. Queste scoperte identificano YAP/TAZ come sensori e mediatori degli stimoli meccanici indotti dal microambinete cellulare.
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Dutour, Provenzano Gaëlle. "Role of intermediate filaments in mechanotransduction." Electronic Thesis or Diss., Sorbonne université, 2021. http://www.theses.fr/2021SORUS364.

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Les cellules s'adaptent en permanence à leur microenvironnement. En particulier, elles modifient leur morphologie, leur croissance, leur division et leur motilité en fonction des propriétés biochimiques et physiques de la matrice extracellulaire (MEC). Elles sont équipées de structures adhésives appelées plaques d’adhérences, permettant aux cellules d'interagir avec les protéines de la MEC via les protéines transmembranaires appelées intégrines et de détecter la nature et la rigidité de la MEC. Le signal est transduit par les protéines des plaques d’adhérences et résulte par exemple en une modification de la tension mécanique induite par l'acto-myosine. Les voies de signalisation en aval peuvent également atteindre le noyau. L'expression des gènes peut alors être modifiée, ce qui peut en retour affecter la composition des plaques d’adhérences et de la MEC pour une réponse cellulaire adaptative. Nous avons émis l'hypothèse qu'en plus des voies de signalisation, un couplage mécanique direct entre les événements se produisant à la périphérie de la cellule et le noyau pourrait participer à la transmission de signaux mécaniques. Bien que les filaments intermédiaires (FIs) aient des propriétés mécaniques extrêmement intéressantes et résistent à des charges de tension élevées, leur implication dans les voies de mécanotransduction est encore mal connue. En utilisant l'astrocyte comme modèle, en raison de sa combinaison spécifique de FIs : vimentine, GFAP, nestine et synémine, nous avons d'abord étudié l'effet de la rigidité du substrat sur la morphologie, la structure et les fonctions du noyau, ainsi que sur l'organisation des FIs autour du noyau. Nous avons ensuite étudié l’impact de l’absence de FI les changements nucléaires observés en réponse à la rigidité du substrat. En utilisant une combinaison de techniques de microfabrication, de méthodes biochimiques et de microscopie, nous avons montré que la rigidité du substrat affecte la forme, le volume du noyau, la structure de la chromatine et le recrutement des facteurs de transcriptions (YAP). Nos résultats suggèrent que les FI forment une structure en forme de cage autour du noyau d'une manière dépendante de la rigidité : un substrat plus rigide induit la formation d’une cage de vimentine et de nestine. Cette interaction avec le noyau pourrait expliquer les modifications nucléaires observées en réponse à la rigidité du substrat. Au total, les résultats obtenus au cours de notre étude permettent de mieux comprendre le rôle des filaments intermédiaires dans les réponses nucléaires aux propriétés mécaniques du substrat
Cells continuously adapt to their microenvironment. In particular, they modulate their morphology, growth, division, and motility according to the biochemical and physical properties of the extracellular matrix (ECM). Cells are equipped with adhesive structures called FAs, allowing them to interact with ECM proteins through the core transmembrane proteins called integrins and to sense the nature and the rigidity of the ECM. This information are transduced by FA proteins and lead, for instance, to changes in acto-myosin-mediated mechanical tension. Downstream signalling pathways also reach the nucleus; gene expression is then modified and may, in return, affect the composition of FAs or of the ECM proteins for adaptative cell response. Here, we hypothesized that, in addition to signalling pathways, a direct mechanical coupling between the events occurring at the cell periphery and the nucleus may participate in the transmission of mechanical cues and the regulation of nuclear functions. Although intermediate filaments (IFs) have extremely interesting mechanical properties and resist high tension load, their involvement in mechanotransduction pathways remains elusive. Using astrocyte as a model, due to its specific combination of IFs: vimentin, GFAP, nestin, and synemin, we studied first the effect of substrate rigidity on the nucleus morphology and function, and on the organisation of IFs around the nucleus. Then, we investigated the role of IFs in rigidity-induced nuclear changes. Using a combination of microfabrication techniques, biochemical and microscopy methods, we showed that substrate rigidity affects the nucleus shape, volume, and structure of the chromatin and the recruitment of transcription factor (YAP) and IFs are mediating these changes. Our results suggest that IFs form a cage-like structure around the nucleus in a rigidity-dependent manner: stiffer substrates promote the formation of a cage of vimentin and nestin. In the absence of IFs, the nuclear changes induced by rigidity are different than with IF. The nucleus increases its size in soft substrate, together with an increase in tension measured by YAP localising in the nucleus. The structure of the chromatin is changed. Altogether, the results obtained during our investigation give a better understanding of the role of intermediate filaments in the mechanosensitive nuclear responses
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Huesa, Carmen. "Mechanotransduction in cells of the osteoblast lineage." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2008. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=25468.

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Books on the topic "Mechanotransduction"

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Mofrad, Mohammad R. K., and Roger D. Kamm, eds. Cellular Mechanotransduction. Cambridge: Cambridge University Press, 2009. http://dx.doi.org/10.1017/cbo9781139195874.

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Matti, Weckström, and Tavi Pasi, eds. Cardiac mechanotransduction. Austin, TX: Landes Bioscience/Eurekah.com, 2007.

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Kamkin, Andre, and Irina Kiseleva, eds. Mechanosensitivity and Mechanotransduction. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-90-481-9881-8.

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Kamkin, Andre. Mechanosensitivity and Mechanotransduction. Dordrecht: Springer Science+Business Media B.V., 2011.

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Xiong, Wei, and Zhigang Xu. Mechanotransduction of the Hair Cell. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-8557-4.

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D, Kamm Roger, ed. Cellular mechanotransduction: Diverse perspectives from molecules to tissues. Cambridge: Cambridge University Press, 2009.

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Chow, Michelle Sze-Weng. The role of focal adhesions in myometrial mechanotransduction. Ottawa: National Library of Canada, 2003.

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Yu-li, Wang, and Discher Dennis E, eds. Cell mechanics. Amsterdam: Elsevier Academic Press, 2007.

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Dionne, Gilman. Structural and Biophysical Studies of Hair Cell Mechanotransduction Proteins. [New York, N.Y.?]: [publisher not identified], 2020.

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Lee, Kristen Lauren. A Mechanism of Mechanotransduction Mediated by the Primary Cilium. [New York, N.Y.?]: [publisher not identified], 2014.

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Book chapters on the topic "Mechanotransduction"

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Gooch, Keith J., and Christopher J. Tennant. "Mechanotransduction." In Mechanical Forces: Their Effects on Cells and Tissues, 123–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-03420-0_6.

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Kim, Sung Soo. "Mechanotransduction, Models." In Encyclopedia of Computational Neuroscience, 1676–83. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6675-8_380.

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Warnock, James N. "Endothelial Mechanotransduction." In Advances in Heart Valve Biomechanics, 37–58. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-01993-8_2.

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Kim, Sung Soo. "Mechanotransduction, Models." In Encyclopedia of Computational Neuroscience, 1–9. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7320-6_380-2.

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Liang, Xin, Landi Sun, and Zhen Liu. "Drosophila Mechanotransduction Channels." In SpringerBriefs in Biochemistry and Molecular Biology, 63–79. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-6526-2_5.

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Leckband, D. E. "Cadherins in Mechanotransduction." In Molecular and Cellular Mechanobiology, 57–80. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-5617-3_3.

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Yip, Kay-Pong, Lavanya Balasubramanian, and James S. K. Sham. "Integrin-Mediated Mechanotransduction in Vascular Smooth Muscle Cells." In Mechanosensitivity and Mechanotransduction, 3–24. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9881-8_1.

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Parker, James C., and Mary I. Townsley. "Control of TRPV4 and Its Effect on the Lung." In Mechanosensitivity and Mechanotransduction, 239–54. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9881-8_10.

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Rubacha, Matthew, and Mingyao Liu. "The Role of Protein-protein Interactions in Mechanotransduction: Implications in Ventilator Induced Lung Injury." In Mechanosensitivity and Mechanotransduction, 255–73. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9881-8_11.

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Young, Suzanne R. L., and Fredrick M. Pavalko. "Cellular Mechanisms of Mechanotransduction in Bone." In Mechanosensitivity and Mechanotransduction, 277–96. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9881-8_12.

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Conference papers on the topic "Mechanotransduction"

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Kaazempur-Mofrad, Mohammad R., Peter J. Mack, Helene Karcher, Javad Golji, and Roger G. Kamm. "Stress-Induced Mechanotransduction: Some Preliminaries." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43215.

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Mechanical stimuli affect nearly every aspect of cellular function, yet the underlying mechanisms of transduction of force into biochemical signals are not clearly understood. One hypothesis is that forces transmitted via individual proteins, either at the site of cell adhesion to its surroundings or within the stress-bearing members of the cytoskeleton, cause conformational changes that change their binding affinity to other intracellular molecules. This altered equilibrium state can subsequently initiate biochemical signaling cascades of produce immediate structural changes. This paper addresses the distribution of forces within the cell resulting from specific mechanical stimuli, computed using a 3-D multi compartment, continuum, viscoelastic finite element model, and uses these to estimate the forces transmitted by individual proteins and protein complexes. These levels of force are compared to those known to produce conformational changes in cytoskeletal proteins, as speculated from magnetocytometry observations and computed by molecular dynamics.
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Wan, Qiaoqiao, Eunhye Cho, Seungman Park, Bumsoo Han, Hiroki Yokota, and Sungsoo Na. "Visualizing Chondrocyte Mechanotransduction in 3D." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14484.

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Chondrocytes are the only cell type present in the articular cartilage and their response to mechanical stimuli influences the maintenance and remodeling of the cartilage. Numerous studies have shown that the balance between anabolic and catabolic responses of the chondrocytes to mechanical loading is dependent on the loading intensities (reviewed in ref. [1]). Moderate, physiological loading, for instance, increases synthetic activity of the extracellular matrix (ECM) such as collagen type II, aggrecan, and proteoglycan, while decreasing the catabolic activity of degradative enzymes such as matrix metalloproteinases (MMPs) and ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) [2,3]. In contrast to moderate loading, static or high-intensity loading has been shown to degrade the cartilage resulting from inhibition of matrix synthesis and up-regulation of catabolic activities [3,4]. Therefore, the importance of these load-dependent signaling pathways involved in the maintenance and remodeling of the cartilage is widely accepted. However, the underlying mechanisms as to how varying magnitudes of mechanical stimuli trigger differential signaling activities that consequently lead to selective gene expression are not clear. FAK and Src are considered to be the main mechanotransduction signaling proteins at the cell-ECM adhesion sites and their activities influence various structural and signaling changes within the cell, including cytoskeletal organization, migration, proliferation, differentiation, and survival [5]. Accumulating evidence has shown that Src and FAK play crucial roles in regulating cartilage maintenance and degeneration and their activation stimulates matrix catabolic genes and activity [6,7]. Rho family GTPases such as RhoA and Rac1 play critical roles in fundamental processes including morphogenesis, polarity, movement, and cell division [8]. They also contribute to cartilage development and degradation [9,10]. Despite these studies, much remains to be elucidated on how load-induced Src and FAK participate in chondrocyte functions, and how their interactions are linked and regulated in connection to the activities of RhoA and Rac1 under different loading conditions. In this study, we use fluorescence resonance energy transfer (FRET)-based biosensors to monitor activities of Src and FAK as well as individual GTPases and evaluate the potential linkage of a network of these signaling molecules under different loading conditions.
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Milewski, Andrew, Dáibhid Ó. Maoiléidigh, and A. J. Hudspeth. "Homeostatic enhancement of active mechanotransduction." In TO THE EAR AND BACK AGAIN - ADVANCES IN AUDITORY BIOPHYSICS: Proceedings of the 13th Mechanics of Hearing Workshop. Author(s), 2018. http://dx.doi.org/10.1063/1.5038515.

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Molladavoodi, Sara, John B. Medley, Maud Gorbet, and H. J. Kwon. "Mechanotransduction in Corneal Epithelial Cells." In ASME 2013 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/imece2013-65406.

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Mechanical properties of the cornea can be affected by diseases such as keratoconus. In keratoconus, a decrease in both thickness and rigidity of the cornea is observed. It is currently not clear whether and how changes in mechanical properties of the cornea are associated with corneal epithelial cell behavior. In the present study, polyacrylamide (PAA) gels with different elastic moduli have been prepared and human corneal epithelial cells (HCECs) have been cultured on them. To investigate the effect that changes in elastic modulus may have on adhesion and migration of corneal epithelial cells, actin filament organization and expression of adhesion molecules were characterized. It was found that HCECs actin filament organization improves with increasing substrate stiffness and integrin α3 expression significantly increases on more compliant substrates.
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Mofrad, Mohammad R. K. "Molecular Mechanosensors and Focal Adhesion Mechanotransduction." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19707.

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Cellular response to mechanical stimulation is mediated by both biochemical mechanisms via changes in gene expression and by biophysical mechanisms via mechanically induced changes in specific molecules’ structure and function. These mechanically responsive molecules can be described as the cell’s mechanosensors and can function to initiate processes such as focal adhesion formation. A series of molecular dynamics investigations explore the mechanosensor function of key molecules involved in focal adhesion formation and cytoskeletal dynamics.
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Warren, Ben. "Unravelling mechanotransduction in the locust ear." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.111920.

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Tamaddoni, Nima, and Stephen A. Sarles. "Mechanotransduction of Multi-Hair Droplet Arrays." In ASME 2014 Conference on Smart Materials, Adaptive Structures and Intelligent Systems. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/smasis2014-7551.

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Early embodiments of droplet interface bilayer (DIB)-based hair cell sensors demonstrated the capability of sensing discrete and continuous perturbations, including single flicks and constant airflow, respectively, of a hair structure that is held in close proximity to a single lipid membrane. In those studies, the use of a single bilayer formed between a pair of droplets provided the necessary environment for studying the physical mechanism of mechanotransduction of a membrane-based sensor as well as the sensitivity and directionality of the assembly. More recently, we showed that additional lipid-coated droplets could be connected in series to form multi-bilayer arrays. Measurements of bilayer current through each interface demonstrated that perturbation of the hair creates a vibration that propagates across several droplets, allowing for the additional interfaces to also sense the perturbation. Depending on the location of the hair in the droplet array, these sensing currents can occur in-phase with one another, allowing for a total sensing current to be easily summed. Two important remaining questions about multi-bilayer arrays include: 1) How is signal propagation affected by the configuration of droplets in the array? 2) How does perturbation of multiple hair structures affect signal propagation and sensing currents in a droplet-array? To study these questions, we form linear series and L-shaped arrays of DIBs where each droplet is instrumented with a sensing electrode. Our experiments show that the motion of the perturbed hair can be transduced by up to three membranes away from the hair and that a change in the orientation of successive interfaces does not significantly affect the propagation of vibrational energy. Separately, experiments on serial arrays with multiple hairs indicate that a second, unperturbed hair does not affect bilayer currents generated by the perturbed hair and that hairs of varying length can add frequency selectivity and stimulus localization capability to multi-bilayer sensors.
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Patel, Sagar S., Ramesh Natarajan, and Rebecca L. Heise. "Mechanotransduction of Primary Cilia in Lung Adenocarcinoma." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80435.

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Lung cancer causes more than 1 million deaths worldwide annually [1]. In a recent study by the American Cancer Society in 2011, more than 221,000 new cases of lung cancers were reported [2]. Out of these, the mortality rate was found in roughly 70% of the cases [2]. Lung cancer is divided into two major categories: small cell and non-small cell. In the United States, non-small cell lung cancer accounts for 85% of all lung cancers and is considered the most common type of lung cancer [2]. It is usually resistant to chemotherapy, therefore making it extremely difficult to treat [3]. Furthermore adenocarcinomas, a type of non-small cell lung cancer, occur towards the periphery of the lungs and are the most common type accounting for 40–45% of all lung cancer cases [3]. Epithelial cells in the healthy lungs undergo stresses during inhalation and expiration of normal breathing. In addition to the forces of normal breathing, lung cancer cells may also experience abnormal mechanical forces due to pre-existing lung diseases such as asthma, bronchitis and chronic obstructive pulmonary disease or other tumor associated structural changes. These conditions can significantly alter the structure of the lungs and cell phenotype [4]. The change in the structure of the lungs affects the mechanical environment of the cells. Changes in extracellular (ECM) stiffness, cell stretch, and shear stress influence tumorigenesis and metastasis [5]. One mechanism through which the cells sense and respond to the cellular mechanical environment is through the primary cilia [6–7]. Primary cilia are non-motile, solitary structures formed from the cellular microtubules and protrude out of each cell. They have also been shown to play an important role in facilitating common cancer signaling pathways such as Sonic Hedgehog and Wnt/β-catenin signaling [8–9]. The objective of this study was to test the hypothesis that lung cancer cells respond to mechanical stimuli with the formation of primary cilia that are necessary for 3 hallmarks of tumor progression: proliferation, epithelial mesenchymal-transition, and migration.
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Holle, Andrew W., Juan Carlos Del Alamo, and Adam J. Engler. "Focal Adhesion Mechanotransduction Regulates Stiffness-Directed Differentiation." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14676.

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Human mesenchymal stem cells (hMSCs) are capable of differentiating into mesodermal lineages, with their fate mirroring the tissue lineage possessing a matching in vivo stiffness. The precise mechanisms responsible for this mechanotransduction-induced change in fate are unknown beyond the requirement for force transmission from the extracellular niche through to the nucleus. As a result of cellular contraction, linker proteins connecting the cytoskeleton to the extracellular matrix (ECM) are exposed to differing levels of force and deform to different extents based on the adjacent ECM’s stiffness. Therefore, some of these linker proteins could act as ‘molecular strain gauges,’ as they have been shown to unfold in response to this force. The unfolding process could result in exposure of cryptic binding sites and induction of new signaling pathways. For example, talin exposes multiple vinculin binding sites under physiological force [1]. Vinculin binds at either end to talin and actin and is thought to change its conformation in conjunction with this force [2] similar to how a strain gauge works. Here we show that force-dependent changes in vinculin recruit MAPK1, inducing a signaling cascade that results in the expression of myogenic markers. Together these data suggest that specific proteins may act as ‘molecular strain gauges’ and play a role in mechanosensitive stem cell differentiation.
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Novak, Caymen, Eric Horst, Ciara Davis, and Geeta Mehta. "Abstract TMIM-080: MECHANOTRANSDUCTION IN OVARIAN CANCERS." In Abstracts: 12th Biennial Ovarian Cancer Research Symposium; September 13-15, 2018; Seattle, Washington. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1557-3265.ovcasymp18-tmim-080.

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