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1
Wyss, Hans M., Joel M. Henderson, Fitzroy J. Byfield, Leslie A. Bruggeman, Yaxian Ding, Chunfa Huang, Jung Hee Suh, et al. "Biophysical properties of normal and diseased renal glomeruli." American Journal of Physiology-Cell Physiology 300, no. 3 (March 2011): C397—C405. http://dx.doi.org/10.1152/ajpcell.00438.2010.
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The mechanical properties of tissues and cells including renal glomeruli are important determinants of their differentiated state, function, and responses to injury but are not well characterized or understood. Understanding glomerular mechanics is important for understanding renal diseases attributable to abnormal expression or assembly of structural proteins and abnormal hemodynamics. We use atomic force microscopy (AFM) and a new technique, capillary micromechanics, to measure the elastic properties of rat glomeruli. The Young's modulus of glomeruli was 2,500 Pa, and it was reduced to 1,100 Pa by cytochalasin and latunculin, and to 1,400 Pa by blebbistatin. Cytochalasin or latrunculin reduced the F/G actin ratios of glomeruli but did not disrupt their architecture. To assess glomerular biomechanics in disease, we measured the Young's moduli of glomeruli from two mouse models of primary glomerular disease, Col4a3−/− mice (Alport model) and Tg26HIV/nl mice (HIV-associated nephropathy model), at stages where glomerular injury was minimal by histopathology. Col4a3−/− mice express abnormal glomerular basement membrane proteins, and Tg26HIV/nl mouse podocytes have multiple abnormalities in morphology, adhesion, and cytoskeletal structure. In both models, the Young's modulus of the glomeruli was reduced by 30%. We find that glomeruli have specific and quantifiable biomechanical properties that are dependent on the state of the actin cytoskeleton and nonmuscle myosins. These properties may be altered early in disease and represent an important early component of disease. This increased deformability of glomeruli could directly contribute to disease by permitting increased distension with hemodynamic force or represent a mechanically inhospitable environment for glomerular cells.
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Kang, Min Kyeong, and Jin-Won Park. "Ectoine Effect on Mechanical Properties of Vesicles in Aqueous Solution." Journal of Membrane Biology 255, no. 1 (November 9, 2021): 55–59. http://dx.doi.org/10.1007/s00232-021-00208-8.
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Park, Jin-Won. "Ca2+-Induced Effect on Mechanical Properties of Sulfatide-Incorporated Vesicles." Journal of Membrane Biology 238, no. 1-3 (November 19, 2010): 63–68. http://dx.doi.org/10.1007/s00232-010-9319-5.
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Soveral *, , R.I. Macey, G. "Mechanical Properties of Brush Border Membrane Vesicles from Kidney Proximal Tubule." Journal of Membrane Biology 158, no. 3 (August 1, 1997): 209–17. http://dx.doi.org/10.1007/s002329900258.
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Zhou, Guoqiao, Bokai Zhang, Liyu Wei, Han Zhang, Massimiliano Galluzzi, and Jiangyu Li. "Spatially Resolved Correlation between Stiffness Increase and Actin Aggregation around Nanofibers Internalized in Living Macrophages." Materials 13, no. 14 (July 21, 2020): 3235. http://dx.doi.org/10.3390/ma13143235.
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Plasticity and functional diversity of macrophages play an important role in resisting pathogens invasion, tumor progression and tissue repair. At present, nanodrug formulations are becoming increasingly important to induce and control the functional diversity of macrophages. In this framework, the internalization process of nanodrugs is co-regulated by a complex interplay of biochemistry, cell physiology and cell mechanics. From a biophysical perspective, little is known about cellular mechanics’ modulation induced by the nanodrug carrier’s internalization. In this study, we used the polylactic-co-glycolic acid (PLGA)–polyethylene glycol (PEG) nanofibers as a model drug carrier, and we investigated their influence on macrophage mechanics. Interestingly, the nanofibers internalized in macrophages induced a local increase of stiffness detected by atomic force microscopy (AFM) nanomechanical investigation. Confocal laser scanning microscopy revealed a thickening of actin filaments around nanofibers during the internalization process. Following geometry and mechanical properties by AFM, indentation experiments are virtualized in a finite element model simulation. It turned out that it is necessary to include an additional actin wrapping layer around nanofiber in order to achieve similar reaction force of AFM experiments, consistent with confocal observation. The quantitative investigation of actin reconfiguration around internalized nanofibers can be exploited to develop novel strategies for drug delivery.
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Wu, Li, Jie Huang, Xiaoxue Yu, Xiaoqing Zhou, Chaoye Gan, Ming Li, and Yong Chen. "AFM of the Ultrastructural and Mechanical Properties of Lipid-Raft-Disrupted and/or Cold-Treated Endothelial Cells." Journal of Membrane Biology 247, no. 2 (January 8, 2014): 189–200. http://dx.doi.org/10.1007/s00232-013-9624-x.
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Loewith, Robbie, Aurélien Roux, and Olivier Pertz. "Chemical-Biology-derived in vivo Sensors: Past, Present, and Future." CHIMIA 75, no. 12 (December 9, 2021): 1017. http://dx.doi.org/10.2533/chimia.2021.1017.
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To understand the complex biochemistry and biophysics of biological systems, one needs to be able to monitor local concentrations of molecules, physical properties of macromolecular assemblies and activation status of signaling pathways, in real time, within single cells, and at high spatio-temporal resolution. Here we look at the tools that have been / are being / need to be provided by chemical biology to address these challenges. In particular, we highlight the utility of molecular probes that help to better measure mechanical forces and flux through key signalling pathways. Chemical biology can be used to both build biosensors to visualize, but also actuators to perturb biological processes. An emergent theme is the possibility to multiplex measurements of multiple cellular processes. Advances in microscopy automation now allow us to acquire datasets for 1000’s of cells. This produces high dimensional datasets that require computer vision approaches that automate image analysis. The high dimensionality of these datasets are often not immediately accessible to human intuition, and, similarly to ‘omics technologies, require statistical approaches for their exploitation. The field of biosensor imaging is therefore experiencing a multidisciplinary transition that will enable it to realize its full potential as a tool to provide a deeper appreciation of cell physiology.
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Chen, Cheng, Dhananjay T. Tambe, Linhong Deng, and Liu Yang. "Biomechanical properties and mechanobiology of the articular chondrocyte." American Journal of Physiology-Cell Physiology 305, no. 12 (December 15, 2013): C1202—C1208. http://dx.doi.org/10.1152/ajpcell.00242.2013.
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To withstand physiological loading over a lifetime, human synovial joints are covered and protected by articular cartilage, a layer of low-friction, load-bearing tissue. The unique mechanical function of articular cartilage largely depends on the composition and structural integrity of the cartilage matrix. The matrix is produced by highly specialized resident cells called chondrocytes. Under physiological loading, chondrocytes maintain the balance between degradation and synthesis of matrix macromolecules. Under excessive loading or injury, however, degradation exceeds synthesis, causing joint degeneration and, eventually, osteoarthritis (OA). Hence, the mechanoresponses of chondrocytes play an important role in the development of OA. Despite its clear importance, the mechanobiology of articular chondrocytes is not well understood. To summarize our current understanding, here we review studies of the effect of mechanical forces on mechanical and biological properties of articular chondrocytes. First, we present the viscoelastic properties of the cell nucleus, chondrocyte, pericellular matrix, and chondron. Then we discuss how these properties change in OA. Finally, we discuss the responses of normal and osteoarthritic chondrocytes to a variety of mechanical stimuli. Studies reviewed here may provide novel insights into the pathogenesis of OA and may help in development of effective biophysical treatment.
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Fay, Meredith E., David R. Myers, Amit Kumar, Rebecca Byler, Todd A. Sulchek, Michael D. Graham, and Wilbur A. Lam. "White Blood Cell Mechanics Mediate Glucocorticoid- and Catecholamine-Induced Demargination." Blood 122, no. 21 (November 15, 2013): 3459. http://dx.doi.org/10.1182/blood.v122.21.3459.3459.
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Abstract After treatment with glucocorticoids (e.g. dexamethasone) or catecholamines (e.g. epinephrine), the white blood cell (WBC) count substantially increases. This is primarily due to WBCs shifting from the marginated to circulating pools (Nakagawa et al., Circulation, 2008) and is traditionally attributed to down-regulation of adhesion molecule expression (Weber et al., J Leukoc Biol, 2004).Recent research has described how mechanical properties determine the radial position of blood cells within the intravascular space (Reasor et. al, Ann Biomed Eng., 2013). In addition, because WBC demargination occurs rapidly (e.g.,<15 min after IV epinephrine infusion (Dimitrov et al., J Immunol. 2010)) on a timescale that may be shorter than that expected for alterations in gene expression, we hypothesized that alterations in WBC mechanical properties upon exposure to glucocorticoids or catecholamines mediate demargination. To that end, we developed an in vitro microfluidic system as a simplified microvasculature model (Fig 1A), which our laboratory has expertise in (Tsai et al., J Clin Invest., 2008 and Rosenbluth et al., Biophys J. , 2006). In the absence of confounding factors such as WBC release from bone marrow or endothelial interactions, this type of assay is ideally suited to determine the role of glucocorticoid and catecholamine treatment on the demargination of WBCs. By flowing whole blood into similar non-functionalized microfluidic devices, other groups have demonstrated that non-activated WBCs marginate to the microfluidic channel wall, which is likely due to their mechanical properties (Jain et al., PLoS One, 2009). Human whole blood was incubated at 37° C with acridine orange (WBC stain) and either dexamethasone or epinephrine at physiologically relevant concentrations. The blood was then flowed through our microfluidics at physiologic shear rates while confocal videomicroscopy was used to image the center plane of the channel. We developed custom analysis software that extracts the position of individual WBCs from a series of confocal images and plots histograms of their locations, tracking over 10,000 WBCs per experiment (Fig 1B). Overall, we found that both dexamethasone and epinephrine (to a slightly lesser extent) cause WBCs to demarginate from the walls of the vessel compared to control conditions (Fig 1C). This glucocorticoid and catecholamine-induced movement of WBCs toward the microchannel center mimics in vivo demargination and our reductionist microfluidic approach strongly suggests that alterations in WBC mechanics play a key role in this process. Indeed, using computational modeling, we confirmed that a reduction in the mechanical stiffness of WBCs is sufficient by itself to explain the observed demargination (Fig 2A) (Kumar et al., Phys Rev Lett., 2012). Using a range of WBC stiffnesses, our simulations revealed that decreases in WBC stiffness correlated with the degree of demargination. To corroborate our microfluidic data, we also directly measured WBC stiffness using atomic force microscopy. WBCs treated with dexamethasone were significantly softer (p< 0.0002) than control WBCs (Fig 2B), supporting our hypothesis that the demargination phenomenon is related to the biophysical changes in WBCs. Experiments measuring the stiffness of epinephrine-treated cells as well as experiments evaluating how these drugs affect the actin cytoskeleton are currently underway. Overall, our data suggest that WBC mechanics play a major role in glucocorticoid- and catecholamine-induced demargination and that the underlying mechanisms may, at least in part, be biophysical in nature. This novel finding may have important implications in other hematologic processes such as WBC margination and recruitment during inflammatory responses or hematopoietic stem cell mobilization and homing. Disclosures: No relevant conflicts of interest to declare.
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Alessandra, Galli, Marku Algerta, Marciani Paola, Schulte Carsten, Lenardi Cristina, Milani Paolo, Maffioli Elisa, Tedeschi Gabriella, and Perego Carla. "Shaping Pancreatic β-Cell Differentiation and Functioning: The Influence of Mechanotransduction." Cells 9, no. 2 (February 11, 2020): 413. http://dx.doi.org/10.3390/cells9020413.
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Embryonic and pluripotent stem cells hold great promise in generating β-cells for both replacing medicine and novel therapeutic discoveries in diabetes mellitus. However, their differentiation in vitro is still inefficient, and functional studies reveal that most of these β-like cells still fail to fully mirror the adult β-cell physiology. For their proper growth and functioning, β-cells require a very specific environment, the islet niche, which provides a myriad of chemical and physical signals. While the nature and effects of chemical stimuli have been widely characterized, less is known about the mechanical signals. We here review the current status of knowledge of biophysical cues provided by the niche where β-cells normally live and differentiate, and we underline the possible machinery designated for mechanotransduction in β-cells. Although the regulatory mechanisms remain poorly understood, the analysis reveals that β-cells are equipped with all mechanosensors and signaling proteins actively involved in mechanotransduction in other cell types, and they respond to mechanical cues by changing their behavior. By engineering microenvironments mirroring the biophysical niche properties it is possible to elucidate the β-cell mechanotransductive-regulatory mechanisms and to harness them for the promotion of β-cell differentiation capacity in vitro.
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Grigg, P. "Biophysical studies of mechanoreceptors." Journal of Applied Physiology 60, no. 4 (April 1, 1986): 1107–15. http://dx.doi.org/10.1152/jappl.1986.60.4.1107.
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Mechanoreception can be viewed as a series of sequential mechanical and ionic processes that take place in mechanosensitive end organs and in the terminals of the nerves that innervate them. Stimuli act on a transducer after being transmitted through some material having a combination of elastic and viscoelastic properties. Channels that open under membrane loading have recently been described in muscle cells and are presented as a model for transduction. When open these channels are cation specific. Ions passing through transducer channels depolarize a spike-initiating zone on the cell. These currents may also activate other conductances in the cell, so that the total generator current may have many components. In many mechanoreceptors, action potential initiation results in activation of an electrogenic Na+ pump at the spike-initiation zone, which modifies the threshold for subsequent action potentials. Action potentials initiated in the many branches of a single sensory axon interact at the branching point of the axon. The rules governing this interaction are complex. The above factors, together or separately, are responsible for the dynamic responses and adaptation observed in mechanoreceptors.
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Ahmed, Adeel, Indranil M. Joshi, Mehran Mansouri, Nuzhet N. N. Ahamed, Meng-Chun Hsu, Thomas R. Gaborski, and Vinay V. Abhyankar. "Engineering fiber anisotropy within natural collagen hydrogels." American Journal of Physiology-Cell Physiology 320, no. 6 (June 1, 2021): C1112—C1124. http://dx.doi.org/10.1152/ajpcell.00036.2021.
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It is well known that biophysical properties of the extracellular matrix (ECM), including stiffness, porosity, composition, and fiber alignment (anisotropy), play a crucial role in controlling cell behavior in vivo. Type I collagen (collagen I) is a ubiquitous structural component in the ECM and has become a popular hydrogel material that can be tuned to replicate the mechanical properties found in vivo. In this review article, we describe popular methods to create 2-D and 3-D collagen I hydrogels with anisotropic fiber architectures. We focus on methods that can be readily translated from engineering and materials science laboratories to the life-science community with the overall goal of helping to increase the physiological relevance of cell culture assays.
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Mohandas, Narla, and Patrick G. Gallagher. "Red cell membrane: past, present, and future." Blood 112, no. 10 (November 15, 2008): 3939–48. http://dx.doi.org/10.1182/blood-2008-07-161166.
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Abstract As a result of natural selection driven by severe forms of malaria, 1 in 6 humans in the world, more than 1 billion people, are affected by red cell abnormalities, making them the most common of the inherited disorders. The non-nucleated red cell is unique among human cell type in that the plasma membrane, its only structural component, accounts for all of its diverse antigenic, transport, and mechanical characteristics. Our current concept of the red cell membrane envisions it as a composite structure in which a membrane envelope composed of cholesterol and phospholipids is secured to an elastic network of skeletal proteins via transmembrane proteins. Structural and functional characterization of the many constituents of the red cell membrane, in conjunction with biophysical and physiologic studies, has led to detailed description of the way in which the remarkable mechanical properties and other important characteristics of the red cells arise, and of the manner in which they fail in disease states. Current studies in this very active and exciting field are continuing to produce new and unexpected revelations on the function of the red cell membrane and thus of the cell in health and disease, and shed new light on membrane function in other diverse cell types.
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Browe, David M., and Clive M. Baumgarten. "Stretch of β1 Integrin Activates an Outwardly Rectifying Chloride Current via FAK and Src in Rabbit Ventricular Myocytes." Journal of General Physiology 122, no. 6 (November 10, 2003): 689–702. http://dx.doi.org/10.1085/jgp.200308899.
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Osmotic swelling of cardiac myocytes and other types of cells activates an outwardly rectifying, tamoxifen-sensitive Cl− current, ICl,swell, but it is unclear whether Cl− currents also are activated by direct mechanical stretch. We tested whether specific stretch of β1-integrin activates a Cl− current in rabbit left ventricular myocytes. Paramagnetic beads (4.5-μm diameter) coated with mAb to β1-integrin were applied to the surface of myocytes and pulled upward with an electromagnet while recording whole-cell current. In solutions designed to isolate anion currents, β1-integrin stretch elicited an outwardly rectifying Cl− current with biophysical and pharmacological properties similar to those of ICl,swell. Stretch-activated Cl− current activated slowly (t1/2 = 3.5 ± 0.1 min), partially inactivated at positive voltages, reversed near ECl, and was blocked by 10 μM tamoxifen. When stretch was terminated, 64 ± 8% of the stretch-induced current reversed within 10 min. Mechanotransduction involved protein tyrosine kinase. Genistein (100 μM), a protein tyrosine kinase inhibitor previously shown to suppress ICl,swell in myocytes, inhibited stretch-activated Cl− current by 62 ± 6% during continued stretch. Because focal adhesion kinase and Src are known to be activated by cell swelling, mechanical stretch, and clustering of integrins, we tested whether these tyrosine kinases mediated the response to β1-integrin stretch. PP2 (10 μM), a selective blocker of focal adhesion kinase and Src, fully inhibited the stretch-activated Cl− current as well as part of the background Cl− current, whereas its inactive analogue PP3 (10 μM) had no significant effect. In addition to activating Cl− current, stretch of β1-integrin also appeared to activate a nonselective cation current and to suppress IK1. Integrins are the primary mechanical link between the extracellular matrix and cytoskeleton. The present results suggest that integrin stretch may contribute to mechano-electric feedback in heart, modulate electrical activity, and influence the propensity for arrhythmogenesis.
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Oakes, Patrick W., Tamara C. Bidone, Yvonne Beckham, Austin V. Skeeters, Guillermina R. Ramirez-San Juan, Stephen P. Winter, Gregory A. Voth, and Margaret L. Gardel. "Lamellipodium is a myosin-independent mechanosensor." Proceedings of the National Academy of Sciences 115, no. 11 (February 27, 2018): 2646–51. http://dx.doi.org/10.1073/pnas.1715869115.
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The ability of adherent cells to sense changes in the mechanical properties of their extracellular environments is critical to numerous aspects of their physiology. It has been well documented that cell attachment and spreading are sensitive to substrate stiffness. Here, we demonstrate that this behavior is actually biphasic, with a transition that occurs around a Young’s modulus of ∼7 kPa. Furthermore, we demonstrate that, contrary to established assumptions, this property is independent of myosin II activity. Rather, we find that cell spreading on soft substrates is inhibited due to reduced myosin-II independent nascent adhesion formation within the lamellipodium. Cells on soft substrates display normal leading-edge protrusion activity, but these protrusions are not stabilized due to impaired adhesion assembly. Enhancing integrin–ECM affinity through addition of Mn2+ recovers nascent adhesion assembly and cell spreading on soft substrates. Using a computational model to simulate nascent adhesion assembly, we find that biophysical properties of the integrin–ECM bond are optimized to stabilize interactions above a threshold matrix stiffness that is consistent with the experimental observations. Together, these results suggest that myosin II-independent forces in the lamellipodium are responsible for mechanosensation by regulating new adhesion assembly, which, in turn, directly controls cell spreading. This myosin II-independent mechanism of substrate stiffness sensing could potentially regulate a number of other stiffness-sensitive processes.
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Wang, Junjie, and Gerhard Dahl. "Pannexin1: a multifunction and multiconductance and/or permeability membrane channel." American Journal of Physiology-Cell Physiology 315, no. 3 (September 1, 2018): C290—C299. http://dx.doi.org/10.1152/ajpcell.00302.2017.
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Of the three pannexins in vertebrate proteomes, pannexin1 (Panx1) is the only one well characterized, and it is generally accepted that Panx1 functions as an ATP release channel for signaling to other cells. However, the ATP permeability of the channel is only observed with certain stimuli, including low oxygen, mechanical stress, and elevated extracellular potassium ion concentration. Otherwise, the Panx1 channel is selective for chloride ions and exhibits no ATP permeability when stimulated simply by depolarization to positive potentials. A third, irreversible activation of Panx1 follows cleavage of carboxyterminal amino acids by caspase 3. The selectivity/permeability properties of the caspase cleaved channel are unclear as it reportedly has features of both channel conformations. Here we describe the biophysical properties of the channel formed by the truncation mutant Panx1Δ378, which is identical to the caspase-cleaved protein. Consistent with previous findings for the caspase-activated channel, the Panx1Δ378 channel was constitutively active. However, like the voltage-gated channel, the Panx1Δ378 channel had high chloride selectivity, lacked cation permeability, and did not mediate ATP release unless stimulated by extracellular potassium ions. Thus, the caspase-cleaved Panx1 channel should be impermeable to ATP, contrary to previous claims.
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Mierke, Claudia Tanja. "Cell Mechanics Drives Migration Modes." Biophysical Reviews and Letters 15, no. 01 (March 2020): 1–34. http://dx.doi.org/10.1142/s1793048020300017.
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The classical migration modes, such as mesenchymal or amoeboid migration modes, are essentially determined by molecular, morphological or biochemical properties of the cells. These specific properties facilitate the cell migration and invasion through artificial extracellular matrices mimicking the environmental conditions of connective tissues. However, during the migration of cells through narrow extracellular matrix constrictions, the specific extracellular matrix environments can either support or impair the invasion of cells. Beyond the classical molecular or biochemical properties, the migration and invasion of cells depends on intracellular cell mechanical characteristics and extracellular matrix mechanical features. The switch between cell states, such as epithelial, mesenchymal or amoeboid states, seems to be mainly based on epigenetic changes and environmental cues that induce the reversible transition of cells toward another state and thereby promote a specific migration mode. However, the exact number of migration modes is not yet clear. Moreover, it is also unclear whether every individual cell, independent of the type, can undergo a transition between all different migration modes in general. A newer theory states that the transition from the jamming to unjamming phase of clustered cells enables cells to migrate as single cells through extracellular matrix confinements. This review will highlight the mechanical features of cells and their matrix environment that regulate and subsequently determine individual migration modes. It is discussed whether each migration mode in each cell type is detectable or whether some migration modes are limited to artificially engineered matrices in vitro and can therefore not or only rarely be detected in vivo. It is specifically pointed out how the intracellular architecture and its contribution to cellular stiffness or contractility favors the employment of a distinct migration mode. Finally, this review envisions a connection between mechanical properties of cells and matrices and the choice of a distinct migration mode in confined 3D microenvironments.
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Isabey, D. "Advances in pulmonary cell mechanics: Mechanical properties, structure and function." Journal of Biomechanics 39 (January 2006): S268. http://dx.doi.org/10.1016/s0021-9290(06)84027-3.
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Obraztsov, Viktor V., Gerald G. Neslund, Elisabeth S. Kornbrust, Stephen F. Flaim, and Catherine M. Woods. "In vitro cellular effects of perfluorochemicals correlate with their lipid solubility." American Journal of Physiology-Lung Cellular and Molecular Physiology 278, no. 5 (May 1, 2000): L1018—L1024. http://dx.doi.org/10.1152/ajplung.2000.278.5.l1018.
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Preclinical studies comparing perflubron partial liquid ventilation with conventional mechanical ventilation have indicated that perflubron partial liquid ventilation may exert some anti-inflammatory effects. To assess whether these effects were related to the lipid solubility properties of perflubron rather than to nonspecific biophysical properties of the perfluorocarbon (PFC) liquid phase, we studied the effects of PFCs with varying lipid solubilities on the platelet aggregation response to various procoagulants and the erythrocyte hemolytic response to osmotic stress. In both cases, the degree of the response was directly related to the lipid solubility of the PFC. All the perflubron content of erythrocytes was found to be associated with the membrane compartment. The time to reach a maximum effect on hemolysis with perflubron was relatively slow (2–4 h), which paralleled the time for perflubron to accumulate in erythrocyte membranes. The rate and extent of perflubron partitioning into lecithin liposomes were similar to those of erythrocyte membranes, supporting the hypothesis that perflubron was partitioning into the lipid component of the membranes. Thus some of the potential modulatory effects of perflubron on excessive inflammatory responses that occur during acute lung injury and acute respiratory distress syndrome may be influenced in part by the extent of PFC partitioning into the lipid bilayers of cellular membranes.
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Blanchoin, Laurent, Rajaa Boujemaa-Paterski, Cécile Sykes, and Julie Plastino. "Actin Dynamics, Architecture, and Mechanics in Cell Motility." Physiological Reviews 94, no. 1 (January 2014): 235–63. http://dx.doi.org/10.1152/physrev.00018.2013.
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Tight coupling between biochemical and mechanical properties of the actin cytoskeleton drives a large range of cellular processes including polarity establishment, morphogenesis, and motility. This is possible because actin filaments are semi-flexible polymers that, in conjunction with the molecular motor myosin, can act as biological active springs or “dashpots” (in laymen's terms, shock absorbers or fluidizers) able to exert or resist against force in a cellular environment. To modulate their mechanical properties, actin filaments can organize into a variety of architectures generating a diversity of cellular organizations including branched or crosslinked networks in the lamellipodium, parallel bundles in filopodia, and antiparallel structures in contractile fibers. In this review we describe the feedback loop between biochemical and mechanical properties of actin organization at the molecular level in vitro, then we integrate this knowledge into our current understanding of cellular actin organization and its physiological roles.
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Vockeroth, Dan, Lasantha Gunasekara, Matthias Amrein, Fred Possmayer, James F. Lewis, and Ruud A. W. Veldhuizen. "Role of cholesterol in the biophysical dysfunction of surfactant in ventilator-induced lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 298, no. 1 (January 2010): L117—L125. http://dx.doi.org/10.1152/ajplung.00218.2009.
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Mechanical ventilation may lead to an impairment of the endogenous surfactant system, which is one of the mechanisms by which this intervention contributes to the progression of acute lung injury. The most extensively studied mechanism of surfactant dysfunction is serum protein inhibition. However, recent studies indicate that hydrophobic components of surfactant may also contribute. It was hypothesized that elevated levels of cholesterol significantly contribute to surfactant dysfunction in ventilation-induced lung injury. Sprague-Dawley rats ( n = 30) were randomized to either high-tidal volume or low-tidal volume ventilation and monitored for 2 h. Subsequently, the lungs were lavaged, surfactant was isolated, and the biophysical properties of this isolated surfactant were analyzed on a captive bubble surfactometer with and without the removal of cholesterol using methyl-β-cyclodextrin. The results showed lower oxygenation values in the high-tidal volume group during the last 30 min of ventilation compared with the low-tidal volume group. Surfactant obtained from the high-tidal volume animals had a significant impairment in function compared with material from the low-tidal volume group. Removal of cholesterol from the high-tidal volume group improved the ability of the surfactant to reduce the surface tension to low values. Subsequent reconstitution of high-cholesterol values led to an impairment in surface activity. It is concluded that increased levels of cholesterol associated with endogenous surfactant represent a major contributor to the inhibition of surfactant function in ventilation-induced lung injury.
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Swerup, C., and B. Rydqvist. "A mathematical model of the crustacean stretch receptor neuron. Biomechanics of the receptor muscle, mechanosensitive ion channels, and macrotransducer properties." Journal of Neurophysiology 76, no. 4 (October 1, 1996): 2211–20. http://dx.doi.org/10.1152/jn.1996.76.4.2211.
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1. A mathematical model of the primary transduction process in a mechanoreceptor, the slowly adapting stretch receptor organ of the crayfish, has been developed taking into account the viscoelastic properties of the accessory structures of the receptor, i.e., the receptor muscle, the biophysical properties of the mechanosensitive channels (MSCs) and the passive electrical properties of the neuronal membrane (leak conductance and capacitative properties). The work is part of an effort to identify and characterize the mechanical and ionic mechanisms in a complex mechanoreceptor. The parameters of the model are based mainly on results of our own experiments and to some extent on results from other studies. The performance of the model has been compared with the performance of the slowly adapting receptor. 2. The model resulted in nonlinear differential equations that were solved by an iterative, fourth order Range-Kutta method. For the calculations of potential, the cell was treated as an idealized spherical body. The extension of the receptor muscle was 0-30%, which is within the physiological limits for this receptor. 3. The mechanical properties of the receptor muscle were modeled by a simple Voigt element (a spring in parallel with a dashpot) in series with a nonlinear spring. This element can describe resonably well the tension development in the receptor muscle at least for large extensions (> 12%). However, for small extensions (< 12%), the muscle seems to be more stiff than for large extensions. 4. The receptor current at different extensions of the receptor was computed using typical viscoelastic parameters for a receptor muscle together with a transformation of muscle tension to tension in the neuronal dendrites and finally the properties of the mechanosensitive channels. The model fit was satisfactory in the high extension range whereas in the low extension range the deviation from the experimental results could be explained partly by insufficient modeling of the nonlinear viscoelastic properties. The voltage dependence of the receptor current was also well predicted by the model. 5. If the parameters of the viscoelastic model were adjusted for each extension so that each tension response closely resembled the experimental values, the fit of the current responses was improved but still deviated from the experimental currents. One factor that might explain the difference is the possibility that the MSCs in the stretch receptor neuron might have intrinsic adaptive properties. Introducing an exponential adaptive behavior of individual MSCs increased the ability of the model to predict the receptor current. 6. The receptor potential was calculated by modeling the neuronal membrane by a lumped leak conductance and capacitance The calculated receptor potential was higher than the experimental receptor potential. However, the fit of the receptor potential was improved substantially by introducing an adaptation of the MSCs as outlined in the preceding paragraph. the remaining discrepancy might be explained by insufficient blocking of K+ channels in the experiment. 7. The model can predict a wide range of experimental data from the slowly adapting stretch receptor neuron including the mechanical response of the receptor muscle, the receptor current and its voltage dependence, and the receptor potential. It also describes accurately the passive electrical properties of the neuronal membrane.
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Ryazantsev, Mikhail N., Dmitrii M. Nikolaev, Andrey V. Struts, and Michael F. Brown. "Quantum Mechanical and Molecular Mechanics Modeling of Membrane-Embedded Rhodopsins." Journal of Membrane Biology 252, no. 4-5 (September 30, 2019): 425–49. http://dx.doi.org/10.1007/s00232-019-00095-0.
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Bidhendi, Amir J., and Anja Geitmann. "Methods to quantify primary plant cell wall mechanics." Journal of Experimental Botany 70, no. 14 (July 1, 2019): 3615–48. http://dx.doi.org/10.1093/jxb/erz281.
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Abstract The primary plant cell wall is a dynamically regulated composite material of multiple biopolymers that forms a scaffold enclosing the plant cells. The mechanochemical make-up of this polymer network regulates growth, morphogenesis, and stability at the cell and tissue scales. To understand the dynamics of cell wall mechanics, and how it correlates with cellular activities, several experimental frameworks have been deployed in recent years to quantify the mechanical properties of plant cells and tissues. Here we critically review the application of biomechanical tool sets pertinent to plant cell mechanics and outline some of their findings, relevance, and limitations. We also discuss methods that are less explored but hold great potential for the field, including multiscale in silico mechanical modeling that will enable a unified understanding of the mechanical behavior across the scales. Our overview reveals significant differences between the results of different mechanical testing techniques on plant material. Specifically, indentation techniques seem to consistently report lower values compared with tensile tests. Such differences may in part be due to inherent differences among the technical approaches and consequently the wall properties that they measure, and partly due to differences between experimental conditions.
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Kuck, Lennart, Jason N. Peart, and Michael J. Simmonds. "Active modulation of human erythrocyte mechanics." American Journal of Physiology-Cell Physiology 319, no. 2 (August 1, 2020): C250—C257. http://dx.doi.org/10.1152/ajpcell.00210.2020.
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The classic view of the red blood cell (RBC) presents a biologically inert cell that upon maturation has limited capacity to alter its physical properties. This view developed largely because of the absence of translational machinery and inability to synthesize or repair proteins in circulating RBC. Recent developments have challenged this perspective, in light of observations supporting the importance of posttranslational modifications and greater understanding of ion movement in these cells, that each regulate a myriad of cellular properties. There is thus now sufficient evidence to induce a step change in understanding of RBC: rather than passively responding to the surrounding environment, these cells have the capacity to actively regulate their physical properties and thus alter flow behavior of blood. Specific evidence supports that the physical and rheological properties of RBC are subject to active modulation, primarily by the second-messenger molecules nitric oxide (NO) and calcium-ions (Ca2+). Furthermore, an isoform of nitric oxide synthase is expressed in RBC (RBC-NOS), which has been recently demonstrated to have an active role in regulating the physical properties of RBC. Mechanical stimulation of the cell membrane activates RBC-NOS, leading to NO generation, which has several intracellular effects, including the S-nitrosylation of integral membrane components. Intracellular concentration of Ca2+ is increased upon mechanical stimulation via the recently identified mechanosensitive cation channel piezo1. Increased intracellular Ca2+ modifies the physical properties of RBC by regulating cell volume and potentially altering several important intracellular proteins. A synthesis of recent advances in understanding of molecular processes within RBC thus challenges the classic view of these cells and rather indicates a highly active cell with self-regulated mechanical properties.
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Emig, Ramona, Callum M. Zgierski-Johnston, Viviane Timmermann, Andrew J. Taberner, Martyn P. Nash, Peter Kohl, and Rémi Peyronnet. "Passive myocardial mechanical properties: meaning, measurement, models." Biophysical Reviews 13, no. 5 (October 2021): 587–610. http://dx.doi.org/10.1007/s12551-021-00838-1.
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AbstractPassive mechanical tissue properties are major determinants of myocardial contraction and relaxation and, thus, shape cardiac function. Tightly regulated, dynamically adapting throughout life, and affecting a host of cellular functions, passive tissue mechanics also contribute to cardiac dysfunction. Development of treatments and early identification of diseases requires better spatio-temporal characterisation of tissue mechanical properties and their underlying mechanisms. With this understanding, key regulators may be identified, providing pathways with potential to control and limit pathological development. Methodologies and models used to assess and mimic tissue mechanical properties are diverse, and available data are in part mutually contradictory. In this review, we define important concepts useful for characterising passive mechanical tissue properties, and compare a variety of in vitro and in vivo techniques that allow one to assess tissue mechanics. We give definitions of key terms, and summarise insight into determinants of myocardial stiffness in situ. We then provide an overview of common experimental models utilised to assess the role of environmental stiffness and composition, and its effects on cardiac cell and tissue function. Finally, promising future directions are outlined.
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Wang, Qianxi, Kawa Manmi, and Kuo-Kang Liu. "Cell mechanics in biomedical cavitation." Interface Focus 5, no. 5 (October 6, 2015): 20150018. http://dx.doi.org/10.1098/rsfs.2015.0018.
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Studies on the deformation behaviours of cellular entities, such as coated microbubbles and liposomes subject to a cavitation flow, become increasingly important for the advancement of ultrasonic imaging and drug delivery. Numerical simulations for bubble dynamics of ultrasound contrast agents based on the boundary integral method are presented in this work. The effects of the encapsulating shell are estimated by adapting Hoff's model used for thin-shell contrast agents. The viscosity effects are estimated by including the normal viscous stress in the boundary condition. In parallel, mechanical models of cell membranes and liposomes as well as state-of-the-art techniques for quantitative measurement of viscoelasticity for a single cell or coated microbubbles are reviewed. The future developments regarding modelling and measurement of the material properties of the cellular entities for cutting-edge biomedical applications are also discussed.
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Haase, Kristina, and Andrew E. Pelling. "Investigating cell mechanics with atomic force microscopy." Journal of The Royal Society Interface 12, no. 104 (March 2015): 20140970. http://dx.doi.org/10.1098/rsif.2014.0970.
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Transmission of mechanical force is crucial for normal cell development and functioning. However, the process of mechanotransduction cannot be studied in isolation from cell mechanics. Thus, in order to understand how cells ‘feel’, we must first understand how they deform and recover from physical perturbations. Owing to its versatility, atomic force microscopy (AFM) has become a popular tool to study intrinsic cellular mechanical properties. Used to directly manipulate and examine whole and subcellular reactions, AFM allows for top-down and reconstitutive approaches to mechanical characterization. These studies show that the responses of cells and their components are complex, and largely depend on the magnitude and time scale of loading. In this review, we generally describe the mechanotransductive process through discussion of well-known mechanosensors. We then focus on discussion of recent examples where AFM is used to specifically probe the elastic and inelastic responses of single cells undergoing deformation. We present a brief overview of classical and current models often used to characterize observed cellular phenomena in response to force. Both simple mechanistic models and complex nonlinear models have been used to describe the observed cellular behaviours, however a unifying description of cell mechanics has not yet been resolved.
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Yalcin, H. C., K. M. Hallow, J. Wang, M. T. Wei, H. D. Ou-Yang, and S. N. Ghadiali. "Influence of cytoskeletal structure and mechanics on epithelial cell injury during cyclic airway reopening." American Journal of Physiology-Lung Cellular and Molecular Physiology 297, no. 5 (November 2009): L881—L891. http://dx.doi.org/10.1152/ajplung.90562.2008.
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Although patients with acute respiratory distress syndrome require mechanical ventilation, these ventilators often exacerbate the existing lung injury. For example, the cyclic closure and reopening of fluid-filled airways during ventilation can cause epithelial cell (EpC) necrosis and barrier disruption. Although much work has focused on minimizing the injurious mechanical forces generated during ventilation, an alternative approach is to make the EpC less susceptible to injury by altering the cell's intrinsic biomechanical/biostructural properties. In this study, we hypothesized that alterations in cytoskeletal structure and mechanics can be used to reduce the cell's susceptibility to injury during airway reopening. EpC were treated with jasplakinolide to stabilize actin filaments or latrunculin A to depolymerize actin and then exposed to cyclic airway reopening conditions at room temperature using a previously developed in vitro cell culture model. Actin stabilization did not affect cell viability but significantly improved cell adhesion primarily due to the development of more numerous focal adhesions. Surprisingly, actin depolymerization significantly improved both cell viability and cell adhesion but weakened focal adhesions. Optical tweezer based measurements of the EpC's micromechanical properties indicate that although latrunculin-treated cells are softer, they also have increased viscous damping properties. To further investigate the effect of “fluidization” on cell injury, experiments were also conducted at 37°C. Although cells held at 37°C exhibited no changes in cytoskeletal structure, they did exhibit increased viscous damping properties and improved cell viability. We conclude that fluidization of the actin cytoskeleton makes the EpC less susceptible to the injurious mechanical forces generated during cyclic airway reopening.
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Gibson, Lorna J. "The hierarchical structure and mechanics of plant materials." Journal of The Royal Society Interface 9, no. 76 (August 8, 2012): 2749–66. http://dx.doi.org/10.1098/rsif.2012.0341.
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The cell walls in plants are made up of just four basic building blocks: cellulose (the main structural fibre of the plant kingdom) hemicellulose, lignin and pectin. Although the microstructure of plant cell walls varies in different types of plants, broadly speaking, cellulose fibres reinforce a matrix of hemicellulose and either pectin or lignin. The cellular structure of plants varies too, from the largely honeycomb-like cells of wood to the closed-cell, liquid-filled foam-like parenchyma cells of apples and potatoes and to composites of these two cellular structures, as in arborescent palm stems. The arrangement of the four basic building blocks in plant cell walls and the variations in cellular structure give rise to a remarkably wide range of mechanical properties: Young's modulus varies from 0.3 MPa in parenchyma to 30 GPa in the densest palm, while the compressive strength varies from 0.3 MPa in parenchyma to over 300 MPa in dense palm. The moduli and compressive strength of plant materials span this entire range. This study reviews the composition and microstructure of the cell wall as well as the cellular structure in three plant materials (wood, parenchyma and arborescent palm stems) to explain the wide range in mechanical properties in plants as well as their remarkable mechanical efficiency.
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Kandel, Judith, Martin Picard, Douglas C. Wallace, and David M. Eckmann. "Mitochondrial DNA 3243A>G heteroplasmy is associated with changes in cytoskeletal protein expression and cell mechanics." Journal of The Royal Society Interface 14, no. 131 (June 2017): 20170071. http://dx.doi.org/10.1098/rsif.2017.0071.
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Mitochondrial and mechanical alterations in cells have both been shown to be hallmarks of human disease. However, little research has endeavoured to establish connections between these two essential features of cells in both functional and dysfunctional situations. In this work, we hypothesized that a specific genetic alteration in mitochondrial function known to cause human disease would trigger changes in cell mechanics. Using a previously characterized set of mitochondrial cybrid cell lines, we examined the relationship between heteroplasmy for the mitochondrial DNA (mtDNA) 3243A>G mutation, the cell cytoskeleton, and resulting cellular mechanical properties. We found that cells with increasing mitochondrial dysfunction markedly differed from one another in gene expression and protein production of various co-regulated cytoskeletal elements. The intracellular positioning and organization of actin also differed across cell lines. To explore the relationship between these changes and cell mechanics, we then measured cellular mechanical properties using atomic force microscopy and found that cell stiffness correlated with gene expression data for known determinants of cell mechanics, γ-actin, α-actinin and filamin A. This work points towards a mechanism linking mitochondrial genetics to single-cell mechanical properties. The transcriptional and structural regulation of cytoskeletal components by mitochondrial function may explain why energetic and mechanical alterations often coexist in clinical conditions.
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Fathi, Ali, Suzanne M. Mithieux, Hua Wei, Wojciech Chrzanowski, Peter Valtchev, Anthony S. Weiss, and Fariba Dehghani. "Elastin based cell-laden injectable hydrogels with tunable gelation, mechanical and biodegradation properties." Biomaterials 35, no. 21 (July 2014): 5425–35. http://dx.doi.org/10.1016/j.biomaterials.2014.03.026.
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Sun, Hongli, Feng Zhu, Qingang Hu, and Paul H. Krebsbach. "Controlling stem cell-mediated bone regeneration through tailored mechanical properties of collagen scaffolds." Biomaterials 35, no. 4 (January 2014): 1176–84. http://dx.doi.org/10.1016/j.biomaterials.2013.10.054.
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Debrah, Dan O., Julianna E. Debrah, Jamie L. Haney, Jonathan T. McGuane, Michael S. Sacks, Kirk P. Conrad, and Sanjeev G. Shroff. "Relaxin regulates vascular wall remodeling and passive mechanical properties in mice." Journal of Applied Physiology 111, no. 1 (July 2011): 260–71. http://dx.doi.org/10.1152/japplphysiol.00845.2010.
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Administration of recombinant human relaxin (rhRLX) to conscious rats increases global arterial compliance, and small renal arteries (SRA) isolated from these rats demonstrate increased passive compliance. Here we characterize relaxin-induced vascular remodeling and examine its functional relevance. SRA and external iliac arteries (EIA) were examined in rhRLX-treated (1.0 μg/h for 5 days) and relaxin knockout mice. Arterial geometric remodeling and compositional remodeling were quantified using immunohistochemical and biochemical techniques. Vascular mechanical properties were quantified using an ex vivo preparation wherein pressure-diameter data were obtained at various axial lengths. Compared with vehicle-treated mice, SRA from rhRLX-treated mice showed outward geometric remodeling (increased unstressed wall area and wall-to-lumen area ratio), increased smooth muscle cell (SMC) density, reduction in collagen-to-total protein ratio, and unchanged elastin-to-tissue dry weight ratio. Compared with wild-type mice, relaxin knockout mice exhibited the opposite pattern: decreased unstressed wall area and wall-to-lumen area ratio, decreased SMC density, and increased collagen-to-total protein ratio. Although tissue biaxial strain energy of SRA was not different between rhRLX- and vehicle-treated groups at low-to-physiological circumferential and axial strains, it was lower for the rhRLX-treated group at the highest circumferential strain. In contrast to SRA, relaxin administration was not associated with any vascular remodeling or changes in passive mechanics of EIA. Thus relaxin induces both geometric and compositional remodeling in vessel-specific manner. Relaxin-induced geometric remodeling of SRA is responsible for the increase in passive compliance under low-to-physiological levels of circumferential and axial strains, and compositional remodeling becomes functionally relevant only under high circumferential strain.
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Cai, Shuang, Lidija Pestic-Dragovich, Martha E. O’Donnell, Ning Wang, Donald Ingber, Elliot Elson, and Primal De Lanerolle. "Regulation of cytoskeletal mechanics and cell growth by myosin light chain phosphorylation." American Journal of Physiology-Cell Physiology 275, no. 5 (November 1, 1998): C1349—C1356. http://dx.doi.org/10.1152/ajpcell.1998.275.5.c1349.
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The role of myosin light chain phosphorylation in regulating the mechanical properties of the cytoskeleton was studied in NIH/3T3 fibroblasts expressing a truncated, constitutively active form of smooth muscle myosin light chain kinase (tMK). Cytoskeletal stiffness determined by quantifying the force required to indent the apical surface of adherent cells showed that stiffness was increased twofold in tMK cells compared with control cells expressing the empty plasmid (Neo cells). Cytoskeletal stiffness quantified using magnetic twisting cytometry showed an ∼1.5-fold increase in stiffness in tMK cells compared with Neo cells. Electronic volume measurements on cells in suspension revealed that tMK cells had a smaller volume and are more resistant to osmotic swelling than Neo cells. tMK cells also have smaller nuclei, and activation of mitogen-activated protein kinase (MAP kinase) and translocation of MAP kinase to the nucleus are slower in tMK cells than in control cells. In tMK cells, there is also less bromodeoxyuridine incorporation, and the doubling time is increased. These data demonstrate that increased myosin light chain phosphorylation correlates with increased cytoskeletal stiffness and suggest that changing the mechanical characteristics of the cytoskeleton alters the intracellular signaling pathways that regulate cell growth and division.
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Tung, Leslie, and Sanjay S. Parikh. "Cardiac Mechanics at the Cellular Level." Journal of Biomechanical Engineering 113, no. 4 (November 1, 1991): 492–95. http://dx.doi.org/10.1115/1.2895431.
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The active mechanical properties of heart muscle are load, length, and time-dependent. The capability for investigating cardiac mechanics at the cellular level may help to distinguish between those properties of the myocardium which arise from myocardial cells and those which arise from the tissue architecture and extracellular matrix of connective fibers. We present here, for the first time, a general approach for subjecting single heart cells to isometric, isotonic, afterloaded, or physiological loading sequences, while obtaining on-line measures of cell force and length. This approach has been implemented and tested on freshly dissociated, adult frog ventricular myocytes. Examples are presented for each of the four loading sequences.
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Rydholm, Susanna, Gordon Zwartz, Jacob M. Kowalewski, Padideh Kamali-Zare, Thomas Frisk, and Hjalmar Brismar. "Mechanical properties of primary cilia regulate the response to fluid flow." American Journal of Physiology-Renal Physiology 298, no. 5 (May 2010): F1096—F1102. http://dx.doi.org/10.1152/ajprenal.00657.2009.
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The primary cilium is a ubiquitous organelle present on most mammalian cells. Malfunction of the organelle has been associated with various pathological disorders, many of which lead to cystic disorders in liver, pancreas, and kidney. Primary cilia have in kidney epithelial cells been observed to generate intracellular calcium in response to fluid flow, and disruption of proteins involved in this calcium signaling lead to autosomal dominant polycystic kidney disease, implying a direct connection between calcium signaling and cyst formation. It has also been shown that there is a significant lag between the onset of flow and initiation of the calcium signal. The present study focuses on the mechanics of cilium bending and the resulting calcium signal. Visualization of real-time cilium movements in response to different types of applied flow showed that the bending is fast compared with the initiation of calcium increase. Mathematical modeling of cilium and surrounding membrane was performed to deduce the relation between bending and membrane stress. The results showed a delay in stress buildup that was similar to the delay in calcium signal. Our results thus indicate that the delay in calcium response upon cilia bending is caused by mechanical properties of the cell membrane.
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Dixon, P. G., and L. J. Gibson. "The structure and mechanics of Moso bamboo material." Journal of The Royal Society Interface 11, no. 99 (October 6, 2014): 20140321. http://dx.doi.org/10.1098/rsif.2014.0321.
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Although bamboo has been used structurally for millennia, there is currently increasing interest in the development of renewable and sustainable structural bamboo products (SBPs). These SBPs are analogous to wood products such as plywood, oriented strand board and glue-laminated wood. In this study, the properties of natural Moso bamboo ( Phyllostachys pubescens ) are investigated to further enable the processing and design of SBPs. The radial and longitudinal density gradients in bamboo give rise to variations in the mechanical properties. Here, we measure the flexural properties of Moso bamboo in the axial direction, along with the compressive strengths in the axial and transverse directions. Based on the microstructural variations (observed with scanning electron microscopy) and extrapolated solid cell wall properties of bamboo, we develop models, which describe the experimental results well. Compared to common North American construction woods loaded along the axial direction, Moso bamboo is approximately as stiff and substantially stronger, in both flexure and compression but denser. This work contributes to critical knowledge surrounding the microstructure and mechanical properties of bamboo, which are vital to the engineering and design of sustainable SBPs.
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Lopez, Michael A., Sherina Bontiff, Mary Adeyeye, Aziz I. Shaibani, Matthew S. Alexander, Shari Wynd, and Aladin M. Boriek. "Mechanics of dystrophin deficient skeletal muscles in very young mice and effects of age." American Journal of Physiology-Cell Physiology 321, no. 2 (August 1, 2021): C230—C246. http://dx.doi.org/10.1152/ajpcell.00155.2019.
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The MDX mouse is an animal model of Duchenne muscular dystrophy, a human disease marked by an absence of the cytoskeletal protein, dystrophin. We hypothesized that 1) dystrophin serves a complex mechanical role in skeletal muscles by contributing to passive compliance, viscoelastic properties, and contractile force production and 2) age is a modulator of passive mechanics of skeletal muscles of the MDX mouse. Using an in vitro biaxial mechanical testing apparatus, we measured passive length-tension relationships in the muscle fiber direction as well as transverse to the fibers, viscoelastic stress-relaxation curves, and isometric contractile properties. To avoid confounding secondary effects of muscle necrosis, inflammation, and fibrosis, we used very young 3-wk-old mice whose muscles reflected the prefibrotic and prenecrotic state. Compared with controls, 1) muscle extensibility and compliance were greater in both along fiber direction and transverse to fiber direction in MDX mice and 2) the relaxed elastic modulus was greater in dystrophin-deficient diaphragms. Furthermore, isometric contractile muscle stress was reduced in the presence and absence of transverse fiber passive stress. We also examined the effect of age on the diaphragm length-tension relationships and found that diaphragm muscles from 9-mo-old MDX mice were significantly less compliant and less extensible than those of muscles from very young MDX mice. Our data suggest that the age of the MDX mouse is a determinant of the passive mechanics of the diaphragm; in the prefibrotic/prenecrotic stage, muscle extensibility and compliance, as well as viscoelasticity, and muscle contractility are altered by loss of dystrophin.
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Bomzon, Ze’ev, Martin M. Knight, Dan L. Bader, and Eitan Kimmel. "Mitochondrial Dynamics in Chondrocytes and Their Connection to the Mechanical Properties of the Cytoplasm." Journal of Biomechanical Engineering 128, no. 5 (February 12, 2006): 674–79. http://dx.doi.org/10.1115/1.2246239.
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Background: The motion and redistribution of intracellular organelles is a fundamental process in cells. Organelle motion is a complex phenomenon that depends on a large number of variables including the shape of the organelle, the type of motors with which the organelles are associated, and the mechanical properties of the cytoplasm. This paper presents a study that characterizes the diffusive motion of mitochondria in chondrocytes seeded in agarose constructs and what this implies about the mechanical properties of the cytoplasm. Method of approach: Images showing mitochondrial motion in individual cells at 30s intervals for 15min were captured with a confocal microscope. Digital image correlation was used to quantify the motion of the mitochondria, and the mean square displacement (MSD) was calculated. Statistical tools for testing whether the characteristic motion of mitochondria varied throughout the cell were developed. Calculations based on statistical mechanics were used to establish connections between the measured MSDs and the mechanical nature of the cytoplasm. Results: The average MSD of the mitochondria varied with time according to a power law with the power term greater than 1, indicating that mitochondrial motion can be viewed as a combination of diffusion and directional motion. Statistical analysis revealed that the motion of the mitochondria was not uniform throughout the cell, and that the diffusion coefficient may vary by over 50%, indicating intracellular heterogeneity. High correlations were found between movements of mitochondria when they were less than 2μm apart. The correlation is probably due to viscoelastic properties of the cytoplasm. Theoretical analysis based on statistical mechanics suggests that directed diffusion can only occur in a material that behaves like a fluid on large time scales. Conclusions: The study shows that mitochondria in different regions of the cell experience different characteristic motions. This suggests that the cytoplasm is a heterogeneous viscoelastic material. The study provides new insight into the motion of mitochondria in chondrocytes and its connection with the mechanical properties of the cytoplasm.
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Bonnet, Isabelle, Philippe Marcq, Floris Bosveld, Luc Fetler, Yohanns Bellaïche, and François Graner. "Mechanical state, material properties and continuous description of an epithelial tissue." Journal of The Royal Society Interface 9, no. 75 (May 23, 2012): 2614–23. http://dx.doi.org/10.1098/rsif.2012.0263.
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During development, epithelial tissues undergo extensive morphogenesis based on coordinated changes of cell shape and position over time. Continuum mechanics describes tissue mechanical state and shape changes in terms of strain and stress. It accounts for individual cell properties using only a few spatially averaged material parameters. To determine the mechanical state and parameters in the Drosophila pupa dorsal thorax epithelium, we severed in vivo the adherens junctions around a disc-shaped domain comprising typically a hundred cells. This enabled a direct measurement of the strain along different orientations at once. The amplitude and the anisotropy of the strain increased during development. We also measured the stress-to-viscosity ratio and similarly found an increase in amplitude and anisotropy. The relaxation time was of the order of 10 s. We propose a space–time, continuous model of the relaxation. Good agreement with experimental data validates the description of the epithelial domain as a continuous, linear, visco-elastic material. We discuss the relevant time and length scales. Another material parameter, the ratio of external friction to internal viscosity, is estimated by fitting the initial velocity profile. Together, our results contribute to quantify forces and displacements, and their time evolution, during morphogenesis.
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Lu, Shing-Hwa, Michael S. Sacks, Steve Y. Chung, D. Claire Gloeckner, Ryan Pruchnic, Johnny Huard, William C. de Groat, and Michael B. Chancellor. "Biaxial mechanical properties of muscle-derived cell seeded small intestinal submucosa for bladder wall reconstitution." Biomaterials 26, no. 4 (February 2005): 443–49. http://dx.doi.org/10.1016/j.biomaterials.2004.05.006.
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Tong, Xinming, and Fan Yang. "Engineering interpenetrating network hydrogels as biomimetic cell niche with independently tunable biochemical and mechanical properties." Biomaterials 35, no. 6 (February 2014): 1807–15. http://dx.doi.org/10.1016/j.biomaterials.2013.11.064.
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Robles, Luis, and Mario A. Ruggero. "Mechanics of the Mammalian Cochlea." Physiological Reviews 81, no. 3 (July 1, 2001): 1305–52. http://dx.doi.org/10.1152/physrev.2001.81.3.1305.
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In mammals, environmental sounds stimulate the auditory receptor, the cochlea, via vibrations of the stapes, the innermost of the middle ear ossicles. These vibrations produce displacement waves that travel on the elongated and spirally wound basilar membrane (BM). As they travel, waves grow in amplitude, reaching a maximum and then dying out. The location of maximum BM motion is a function of stimulus frequency, with high-frequency waves being localized to the “base” of the cochlea (near the stapes) and low-frequency waves approaching the “apex” of the cochlea. Thus each cochlear site has a characteristic frequency (CF), to which it responds maximally. BM vibrations produce motion of hair cell stereocilia, which gates stereociliar transduction channels leading to the generation of hair cell receptor potentials and the excitation of afferent auditory nerve fibers. At the base of the cochlea, BM motion exhibits a CF-specific and level-dependent compressive nonlinearity such that responses to low-level, near-CF stimuli are sensitive and sharply frequency-tuned and responses to intense stimuli are insensitive and poorly tuned. The high sensitivity and sharp-frequency tuning, as well as compression and other nonlinearities (two-tone suppression and intermodulation distortion), are highly labile, indicating the presence in normal cochleae of a positive feedback from the organ of Corti, the “cochlear amplifier.” This mechanism involves forces generated by the outer hair cells and controlled, directly or indirectly, by their transduction currents. At the apex of the cochlea, nonlinearities appear to be less prominent than at the base, perhaps implying that the cochlear amplifier plays a lesser role in determining apical mechanical responses to sound. Whether at the base or the apex, the properties of BM vibration adequately account for most frequency-specific properties of the responses to sound of auditory nerve fibers.
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An, Steven S., and Jeffrey J. Fredberg. "Biophysical basis for airway hyperresponsivenessThis article is one of a selection of papers published in the Special Issue on Recent Advances in Asthma Research." Canadian Journal of Physiology and Pharmacology 85, no. 7 (July 2007): 700–714. http://dx.doi.org/10.1139/y07-059.
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Airway hyperresponsiveness is the excessive narrowing of the airway lumen caused by stimuli that would cause little or no narrowing in the normal individual. It is one of the cardinal features of asthma, but its mechanisms remain unexplained. In asthma, the key end-effector of acute airway narrowing is contraction of the airway smooth muscle cell that is driven by myosin motors exerting their mechanical effects within an integrated cytoskeletal scaffolding. In just the past few years, however, our understanding of the rules that govern muscle biophysics has dramatically changed, as has their classical relationship to airway mechanics. It has become well established, for example, that muscle length is equilibrated dynamically rather than statically, and that in a dynamic setting nonclassical features of muscle biophysics come to the forefront, including unanticipated interactions between the muscle and its time-varying load, as well as the ability of the muscle cell to adapt (remodel) its internal microstructure rapidly in response to its ever-changing mechanical environment. Here, we consider some of these emerging concepts and, in particular, focus on structural remodeling of the airway smooth muscle cell as it relates to excessive airway narrowing in asthma.
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Shi, Yu, Shankar Sivarajan, Katherine M. Xiang, Geran M. Kostecki, Leslie Tung, John C. Crocker, and Daniel H. Reich. "Pervasive cytoquakes in the actomyosin cortex across cell types and substrate stiffness." Integrative Biology 13, no. 10 (October 2021): 246–57. http://dx.doi.org/10.1093/intbio/zyab017.
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Abstract The actomyosin cytoskeleton enables cells to resist deformation, crawl, change their shape and sense their surroundings. Despite decades of study, how its molecular constituents can assemble together to form a network with the observed mechanics of cells remains poorly understood. Recently, it has been shown that the actomyosin cortex of quiescent cells can undergo frequent, abrupt reconfigurations and displacements, called cytoquakes. Notably, such fluctuations are not predicted by current physical models of actomyosin networks, and their prevalence across cell types and mechanical environments has not previously been studied. Using micropost array detectors, we have performed high-resolution measurements of the dynamic mechanical fluctuations of cells’ actomyosin cortex and stress fiber networks. This reveals cortical dynamics dominated by cytoquakes—intermittent events with a fat-tailed distribution of displacements, sometimes spanning microposts separated by 4 μm, in all cell types studied. These included 3T3 fibroblasts, where cytoquakes persisted over substrate stiffnesses spanning the tissue-relevant range of 4.3 kPa–17 kPa, and primary neonatal rat cardiac fibroblasts and myofibroblasts, human embryonic kidney cells and human bone osteosarcoma epithelial (U2OS) cells, where cytoquakes were observed on substrates in the same stiffness range. Overall, these findings suggest that the cortex self-organizes into a marginally stable mechanical state whose physics may contribute to cell mechanical properties, active behavior and mechanosensing.
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Chan, C. J., G. Whyte, L. Boyde, G. Salbreux, and J. Guck. "Impact of heating on passive and active biomechanics of suspended cells." Interface Focus 4, no. 2 (April 6, 2014): 20130069. http://dx.doi.org/10.1098/rsfs.2013.0069.
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A cell is a complex material whose mechanical properties are essential for its normal functions. Heating can have a dramatic effect on these mechanical properties, similar to its impact on the dynamics of artificial polymer networks. We investigated such mechanical changes by the use of a microfluidic optical stretcher, which allowed us to probe cell mechanics when the cells were subjected to different heating conditions at different time scales. We find that HL60/S4 myeloid precursor cells become mechanically more compliant and fluid-like when subjected to either a sudden laser-induced temperature increase or prolonged exposure to higher ambient temperature. Above a critical temperature of 52 ± 1°C, we observed active cell contraction, which was strongly correlated with calcium influx through temperature-sensitive transient receptor potential vanilloid 2 (TRPV2) ion channels, followed by a subsequent expansion in cell volume. The change from passive to active cellular response can be effectively described by a mechanical model incorporating both active stress and viscoelastic components. Our work highlights the role of TRPV2 in regulating the thermomechanical response of cells. It also offers insights into how cortical tension and osmotic pressure govern cell mechanics and regulate cell-shape changes in response to heat and mechanical stress.
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Dailey, H. L., L. M. Ricles, H. C. Yalcin, and S. N. Ghadiali. "Image-based finite element modeling of alveolar epithelial cell injury during airway reopening." Journal of Applied Physiology 106, no. 1 (January 2009): 221–32. http://dx.doi.org/10.1152/japplphysiol.90688.2008.
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The acute respiratory distress syndrome (ARDS) is characterized by fluid accumulation in small pulmonary airways. The reopening of these fluid-filled airways involves the propagation of an air-liquid interface that exerts injurious hydrodynamic stresses on the epithelial cells (EpC) lining the airway walls. Previous experimental studies have demonstrated that these hydrodynamic stresses may cause rupture of the plasma membrane (i.e., cell necrosis) and have postulated that cell morphology plays a role in cell death. However, direct experimental measurement of stress and strain within the cell is intractable, and limited data are available on the mechanical response (i.e., deformation) of the epithelium during airway reopening. The goal of this study is to use image-based finite element models of cell deformation during airway reopening to investigate how cell morphology and mechanics influence the risk of cell injury/necrosis. Confocal microscopy images of EpC in subconfluent and confluent monolayers were used to generate morphologically accurate three-dimensional finite element models. Hydrodynamic stresses on the cells were calculated from boundary element solutions of bubble propagation in a fluid-filled parallel-plate flow channel. Results indicate that for equivalent cell mechanical properties and hydrodynamic load conditions, subconfluent cells develop higher membrane strains than confluent cells. Strain magnitudes were also found to decrease with increasing stiffness of the cell and membrane/cortex region but were most sensitive to changes in the cell's interior stiffness. These models may be useful in identifying pharmacological treatments that mitigate cell injury during airway reopening by altering specific biomechanical properties of the EpC.
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MacQueen, Luke, Yu Sun, and Craig A. Simmons. "Mesenchymal stem cell mechanobiology and emerging experimental platforms." Journal of The Royal Society Interface 10, no. 84 (July 6, 2013): 20130179. http://dx.doi.org/10.1098/rsif.2013.0179.
Full textAbstract:
Experimental control over progenitor cell lineage specification can be achieved by modulating properties of the cell's microenvironment. These include physical properties of the cell adhesion substrate, such as rigidity, topography and deformation owing to dynamic mechanical forces. Multipotent mesenchymal stem cells (MSCs) generate contractile forces to sense and remodel their extracellular microenvironments and thereby obtain information that directs broad aspects of MSC function, including lineage specification. Various physical factors are important regulators of MSC function, but improved understanding of MSC mechanobiology requires novel experimental platforms. Engineers are bridging this gap by developing tools to control mechanical factors with improved precision and throughput, thereby enabling biological investigation of mechanics-driven MSC function. In this review, we introduce MSC mechanobiology and review emerging cell culture platforms that enable new insights into mechanobiological control of MSCs. Our main goals are to provide engineers and microtechnology developers with an up-to-date description of MSC mechanobiology that is relevant to the design of experimental platforms and to introduce biologists to these emerging platforms.
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Movilla, Nieves, Clara Valero, Carlos Borau, and Jose Manuel García-Aznar. "Matrix degradation regulates osteoblast protrusion dynamics and individual migration." Integrative Biology 11, no. 11 (November 2019): 404–13. http://dx.doi.org/10.1093/intbio/zyz035.
Full textAbstract:
Abstract Protrusions are one of the structures that cells use to sense their surrounding environment in a probing and exploratory manner as well as to communicate with other cells. In particular, osteoblasts embedded within a 3D matrix tend to originate a large number of protrusions compared to other type of cells. In this work, we study the role that mechanochemical properties of the extracellular matrix (ECM) play on the dynamics of these protrusions, namely, the regulation of the size and number of emanating structures. In addition, we also determine how the dynamics of the protrusions may lead the 3D movement of the osteoblasts. Significant differences were found in protrusion size and cell velocity, when degradation activity due to metalloproteases was blocked by means of an artificial broad-spectrum matrix metalloproteinase inhibitor, whereas stiffening of the matrix by introducing transglutaminase crosslinking, only induced slight changes in both protrusion size and cell velocity, suggesting that the ability of cells to create a path through the matrix is more critical than the matrix mechanical properties themselves. To confirm this, we developed a cell migration computational model in 3D including both the mechanical and chemical properties of the ECM as well as the protrusion mechanics, obtaining good agreement with experimental results.