Journal articles: 'Cytoskeleton model'

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Durand-Smet, Pauline, Tamsin A. Spelman, Elliot M. Meyerowitz, and Henrik Jönsson. "Cytoskeletal organization in isolated plant cells under geometry control." Proceedings of the National Academy of Sciences 117, no. 29 (July 8, 2020): 17399–408. http://dx.doi.org/10.1073/pnas.2003184117.

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The cytoskeleton plays a key role in establishing robust cell shape. In animals, it is well established that cell shape can also influence cytoskeletal organization. Cytoskeletal proteins are well conserved between animal and plant kingdoms; nevertheless, because plant cells exhibit major structural differences to animal cells, the question arises whether the plant cytoskeleton also responds to geometrical cues. Recent numerical simulations predicted that a geometry-based rule is sufficient to explain the microtubule (MT) organization observed in cells. Due to their high flexural rigidity and persistence length of the order of a few millimeters, MTs are rigid over cellular dimensions and are thus expected to align along their long axis if constrained in specific geometries. This hypothesis remains to be testedin cellulo. Here, we explore the relative contribution of geometry to the final organization of actin and MT cytoskeletons in single plant cells ofArabidopsis thaliana. We show that the cytoskeleton aligns with the long axis of the cells. We find that actin organization relies on MTs but not the opposite. We develop a model of self-organizing MTs in three dimensions, which predicts the importance of MT severing, which we confirm experimentally. This work is a first step toward assessing quantitatively how cellular geometry contributes to the control of cytoskeletal organization in living plant cells.

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Akram, Zain, Ishtiaq Ahmed, Heike Mack, Ramandeep Kaur, Richard C. Silva, Beatriz A. Castilho, Sylvie Friant, Evelyn Sattlegger, and Alan L. Munn. "Yeast as a Model to Understand Actin-Mediated Cellular Functions in Mammals—Illustrated with Four Actin Cytoskeleton Proteins." Cells 9, no. 3 (March 10, 2020): 672. http://dx.doi.org/10.3390/cells9030672.

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The budding yeast Saccharomyces cerevisiae has an actin cytoskeleton that comprises a set of protein components analogous to those found in the actin cytoskeletons of higher eukaryotes. Furthermore, the actin cytoskeletons of S. cerevisiae and of higher eukaryotes have some similar physiological roles. The genetic tractability of budding yeast and the availability of a stable haploid cell type facilitates the application of molecular genetic approaches to assign functions to the various actin cytoskeleton components. This has provided information that is in general complementary to that provided by studies of the equivalent proteins of higher eukaryotes and hence has enabled a more complete view of the role of these proteins. Several human functional homologues of yeast actin effectors are implicated in diseases. A better understanding of the molecular mechanisms underpinning the functions of these proteins is critical to develop improved therapeutic strategies. In this article we chose as examples four evolutionarily conserved proteins that associate with the actin cytoskeleton: (1) yeast Hof1p/mammalian PSTPIP1, (2) yeast Rvs167p/mammalian BIN1, (3) yeast eEF1A/eEF1A1 and eEF1A2 and (4) yeast Yih1p/mammalian IMPACT. We compare the knowledge on the functions of these actin cytoskeleton-associated proteins that has arisen from studies of their homologues in yeast with information that has been obtained from in vivo studies using live animals or in vitro studies using cultured animal cell lines.

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Wang, Jizeng, and Long Li. "Coupled elasticity–diffusion model for the effects of cytoskeleton deformation on cellular uptake of cylindrical nanoparticles." Journal of The Royal Society Interface 12, no. 102 (January 2015): 20141023. http://dx.doi.org/10.1098/rsif.2014.1023.

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Molecular dynamic simulations and experiments have recently demonstrated how cylindrical nanoparticles (CNPs) with large aspect ratios penetrate animal cells and inevitably deform cytoskeletons. Thus, a coupled elasticity–diffusion model was adopted to elucidate this interesting biological phenomenon by considering the effects of elastic deformations of cytoskeleton and membrane, ligand–receptor binding and receptor diffusion. The mechanism by which the binding energy drives the CNPs with different orientations to enter host cells was explored. This mechanism involved overcoming the resistance caused by cytoskeleton and membrane deformations and the change in configurational entropy of the ligand–receptor bonds and free receptors. Results showed that deformation of the cytoskeleton significantly influenced the engulfing process by effectively slowing down and even hindering the entry of the CNPs. Additionally, the engulfing depth was determined quantitatively. CNPs preferred or tended to vertically attack target cells until they were stuck in the cytoskeleton as implied by the speed of vertically oriented CNPs that showed much faster initial engulfing speeds than horizontally oriented CNPs. These results elucidated the most recent molecular dynamics simulations and experimental observations on the cellular uptake of carbon nanotubes and phagocytosis of filamentous Escherichia coli bacteria. The most efficient engulfment showed the stiffness-dependent optimal radius of the CNPs. Cytoskeleton stiffness exhibited more significant influence on the optimal sizes of the vertical uptake than the horizontal uptake.

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Ning, Liang, Hani Y. Suleiman, and Jeffrey H. Miner. "Synaptopodin deficiency exacerbates kidney disease in a mouse model of Alport syndrome." American Journal of Physiology-Renal Physiology 321, no. 1 (July 1, 2021): F12—F25. http://dx.doi.org/10.1152/ajprenal.00035.2021.

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Alport syndrome (AS) is a hereditary disease of the glomerular basement with hematuria and proteinuria. Podocytes eventually exhibit foot process effacement, indicating actin cytoskeletal changes. To investigate how cytoskeletal changes impact podocytes, we generated Alport mice lacking synaptopodin, an actin-binding protein in foot processes. Analysis showed a more rapid disease progression, demonstrating that synaptopodin is protective. This suggests that the actin cytoskeleton is a target for therapy in AS and perhaps other glomerular diseases.

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REDONDO, Pedro C., Ana I. LAJAS, Ginés M. SALIDO, Antonio GONZALEZ, Juan A. ROSADO, and José A. PARIENTE. "Evidence for secretion-like coupling involving pp60src in the activation and maintenance of store-mediated Ca2+ entry in mouse pancreatic acinar cells." Biochemical Journal 370, no. 1 (February 15, 2003): 255–63. http://dx.doi.org/10.1042/bj20021505.

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Store-mediated Ca2+ entry (SMCE) is one of the main pathways for Ca2+ influx in non-excitable cells. Recent studies favour a secretion-like coupling mechanism to explain SMCE, where Ca2+ entry is mediated by an interaction of the endoplasmic reticulum (ER) with the plasma membrane (PM) and is modulated by the actin cytoskeleton. To explore this possibility further we have now investigated the role of the actin cytoskeleton in the activation and maintenance of SMCE in pancreatic acinar cells, a more specialized secretory cell type which might be an ideal cellular model to investigate further the properties of the secretion-like coupling model. In these cells, the cytoskeletal disrupters cytochalasin D and latrunculin A inhibited both the activation and maintenance of SMCE. In addition, stabilization of a cortical actin barrier by jasplakinolide prevented the activation, but not the maintenance, of SMCE, suggesting that, as for secretion, the actin cytoskeleton plays a double role in SMCE as a negative modulator of the interaction between the ER and PM, but is also required for this mechanism, since the cytoskeleton disrupters impaired Ca2+ entry. Finally, depletion of the intracellular Ca2+ stores induces cytoskeletal association and activation of pp60src, which is independent on Ca2+ entry. pp60src activation requires the integrity of the actin cytoskeleton and participates in the initial phase of the activation of SMCE in pancreatic acinar cells.

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Jean, Ronald P., Christopher S. Chen, and Alexander A. Spector. "Finite-Element Analysis of the Adhesion-Cytoskeleton-Nucleus Mechanotransduction Pathway During Endothelial Cell Rounding: Axisymmetric Model." Journal of Biomechanical Engineering 127, no. 4 (January 20, 2005): 594–600. http://dx.doi.org/10.1115/1.1933997.

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Endothelial cells possess a mechanical network connecting adhesions on the basal surface, the cytoskeleton, and the nucleus. Transmission of force at adhesions via this pathway can deform the nucleus, ultimately resulting in an alteration of gene expression and other cellular changes (mechanotransduction). Previously, we measured cell adhesion area and apparent nuclear stretch during endothelial cell rounding. Here, we reconstruct the stress map of the nucleus from the observed strains using finite-element modeling. To simulate the disruption of adhesions, we prescribe displacement boundary conditions at the basal surface of the axisymmetric model cell. We consider different scenarios of the cytoskeletal arrangement, and represent the cytoskeleton as either discrete fibers or as an effective homogeneous layer. When the nucleus is in the initial (spread) state, cytoskeletal tension holds the nucleus in an elongated, ellipsoidal configuration. Loss of cytoskeletal tension during cell rounding is represented by reactive forces acting on the nucleus in the model. In our simulations of cell rounding, we found that, for both representations of the cytoskeleton, the loss of cytoskeletal tension contributed more to the observed nuclear deformation than passive properties. Since the simulations make no assumption about the heterogeneity of the nucleus, the stress components both within and on the surface of the nucleus were calculated. The nuclear stress map showed that the nucleus experiences stress on the order of magnitude that can be significant for the function of DNA molecules and chromatin fibers. This study of endothelial cell mechanobiology suggests the possibility that mechanotransduction could result, in part, from nuclear deformation, and may be relevant to angiogenesis, wound healing, and endothelial barrier dysfunction.

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Symington, Alison L., Selma Zimmerman, and A. M. Zimmerman. "The influence of hydrostatic pressure on the distribution of histone mRNA in HeLa cells." Biochemistry and Cell Biology 71, no. 3-4 (March 1, 1993): 150–55. http://dx.doi.org/10.1139/o93-024.

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Hydrostatic pressure and HeLa S3 cells were used (as a model system) to investigate the relationship of the cytoskeleton and histone gene expression. Exposure of HeLa S3 cells to hydrostatic pressure of 1000 – 10 000 psi (6.89 × 103 – 6.89 × 104 kPa) disrupts the cytoskeleton and reduces H1 and core histone mRNA and actin mRNA levels as determined by hybridization to specific DNA probes. Soluble and insoluble cell fractions were isolated from HeLa cells after lysis in Triton X-100 buffered with PIPES and being subjected to low-speed centrifugation. The insoluble fraction was designated the cytoskeletal fraction. At atmospheric pressure, 76% of H4 histone mRNA is associated with the cytoskeletal fraction and 24% of the H4 histone mRNA is in the soluble fraction. At 6000 and 10 000 psi for a duration of 10 min, H4 mRNA levels in the cytoskeletal fraction were reduced to 52 and 41%, respectively. The reduction of mRNA in the cytoskeletal fraction is accompanied by a corresponding increase of mRNA in the soluble cell fraction. The other core (H2A, H2B, and H3) and H1 histone mRNA transcripts exhibited similar sensitivity to pressure treatment. The effects of pressure on histone gene regulation may be mediated through alteration of mRNA–cytoskeleton association.Key words: cytoskeleton, HeLa cells, histone mRNA, hydrostatic pressure.

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Clark, J. I., J. M. Clark, L. L. David, and H. Matsushima. "Lens cytoskeleton and transparency: A model." Eye 13, no. 3 (May 1999): 417–24. http://dx.doi.org/10.1038/eye.1999.116.

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Liu, Fei, Dan Wu, Xiaoyong Wu, and Ken Chen. "Analyses of the cell mechanical damage during microinjection." Soft Matter 11, no. 7 (2015): 1434–42. http://dx.doi.org/10.1039/c4sm02773f.

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The structure of the cell mechanical model. The cell model contains the membrane networks, the internal cytoskeleton, ACPs, motors and their functions, including the binding/unbinding and the folding/unfolding of the proteins, the polymerization/depolymerization of cytoskeletal filaments, and the walk of motors.

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Dufort, Paul A., and Charles J. Lumsden. "Cellular automaton model of the actin cytoskeleton." Cell Motility and the Cytoskeleton 25, no. 1 (1993): 87–104. http://dx.doi.org/10.1002/cm.970250110.

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Xu, Jian-Wei, Bo Cheng, Yu-Yu Feng, Zi-Qing Wang, and Guo-Dong Wang. "Cytoskeleton Dynamics: A Continuum Cooperative Hydrolysis Model." Communications in Theoretical Physics 63, no. 5 (May 1, 2015): 648–52. http://dx.doi.org/10.1088/0253-6102/63/5/648.

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Regalado, Carlos M., Brian D. Sleeman, and Karl Ritz. "Aggregation and collapse of fungal wall vesicles in hyphal tips: a model for the origin of the Spitzenkörper." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 352, no. 1364 (December 29, 1997): 1963–74. http://dx.doi.org/10.1098/rstb.1997.0182.

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The intracellular origins of polarity and branch initiation in fungi centre upon a localization in the supply of fungal wall constituents to specific regions on the hyphal wall. Polarity is achieved and maintained by accumulating secretory vesicles, prior to incorporation into the wall, in the form of an apical body or Spitzenkörper. However, neither the mechanisms leading to this accumulation nor the initiation of branching, are as yet understood. We propose a mechanism, based on experimental evidence, which considers the mechanical properties of the cytoskeleton in order to explain these phenomena. Cytoskeletal viscoelastic forces are hypothesized to be responsible for biasing vesicles in their motion, and a mathematical model is derived to take these considerations into account. We find that, as a natural consequence of the assumed interactions between vesicles and cytoskeleton, wall vesicles aggregate in a localized region close to the tip apex. These results are used to interpret the origin of the Spitzenkörper. The model also shows that an aggregation peak can collapse and give rise to two new centres of aggregation coexisting near the tip. We interpret this as a mechanism for apical branching, in agreement with published observations. We also investigate the consequences and presumptive role of vesicle—cytoskeleton interactions in the migration of satellite Spitzenkörper. The results of this work strongly suggest that the formation of the Spitzenkörper and the series of dynamical events leading to hyphal branching arise as a consequence of the bias in vesicle motion resulting from interactions with the cytoskeleton.

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Shafrir, Yinon, and Gabor Forgacs. "Mechanotransduction through the cytoskeleton." American Journal of Physiology-Cell Physiology 282, no. 3 (March 1, 2002): C479—C486. http://dx.doi.org/10.1152/ajpcell.00394.2001.

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We constructed a model cytoskeleton to investigate the proposal that this interconnected filamentous structure can act as a mechano- and signal transducer. The model cytoskeleton is composed of rigid rods representing actin filaments, which are connected with springs representing cross-linker molecules. The entire mesh is placed in viscous cytoplasm. The model eukaryotic cell is submitted to either shock wave-like or periodic mechanical perturbations at its membrane. We calculated the efficiency of this network to transmit energy to the nuclear wall as a function of cross-linker stiffness, cytoplasmic viscosity, and external stimulation frequency. We found that the cytoskeleton behaves as a tunable band filter: for given linker molecules, energy transmission peaks in a narrow range of stimulation frequencies. Most of the normal modes of the network are spread over the same frequency range. Outside this range, signals are practically unable to reach their destination. Changing the cellular ratios of linker molecules with different elastic characteristics can control the allowable frequency range and, with it, the efficiency of mechanotransduction.

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Heidemann, Steven R., Stefanie Kaech, Robert E. Buxbaum, and Andrew Matus. "Direct Observations of the Mechanical Behaviors of the Cytoskeleton in Living Fibroblasts." Journal of Cell Biology 145, no. 1 (April 5, 1999): 109–22. http://dx.doi.org/10.1083/jcb.145.1.109.

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Cytoskeletal proteins tagged with green fluorescent protein were used to directly visualize the mechanical role of the cytoskeleton in determining cell shape. Rat embryo (REF 52) fibroblasts were deformed using glass needles either uncoated for purely physical manipulations, or coated with laminin to induce attachment to the cell surface. Cells responded to uncoated probes in accordance with a three-layer model in which a highly elastic nucleus is surrounded by cytoplasmic microtubules that behave as a jelly-like viscoelastic fluid. The third, outermost cortical layer is an elastic shell under sustained tension. Adhesive, laminin-coated needles caused focal recruitment of actin filaments to the contacted surface region and increased the cortical layer stiffness. This direct visualization of actin recruitment confirms a widely postulated model for mechanical connections between extracellular matrix proteins and the actin cytoskeleton. Cells tethered to laminin-treated needles strongly resisted elongation by actively contracting. Whether using uncoated probes to apply simple deformations or laminin-coated probes to induce surface-to-cytoskeleton interaction we observed that experimentally applied forces produced exclusively local responses by both the actin and microtubule cytoskeleton. This local accomodation and dissipation of force is inconsistent with the proposal that cellular tensegrity determines cell shape.

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Copos, Calina Anamaria, and Robert D. Guy. "A porous viscoelastic model for the cell cytoskeleton." ANZIAM Journal 59 (August 9, 2018): 472. http://dx.doi.org/10.21914/anziamj.v59i0.12339.

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COPOS, CALINA A., and ROBERT D. GUY. "A POROUS VISCOELASTIC MODEL FOR THE CELL CYTOSKELETON." ANZIAM Journal 59, no. 4 (April 2018): 472–98. http://dx.doi.org/10.1017/s1446181118000081.

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The immersed boundary method is a widely used mixed Eulerian/Lagrangian framework for simulating the motion of elastic structures immersed in viscous fluids. In this work, we consider a poroelastic immersed boundary method in which a fluid permeates a porous, elastic structure of negligible volume fraction, and extend this method to include stress relaxation of the material. The porous viscoelastic method presented here is validated for a prescribed oscillatory shear and for an expansion driven by the motion at the boundary of a circular material by comparing numerical solutions to an analytical solution of the Maxwell model for viscoelasticity. Finally, an application of the modelling framework to cell biology is provided: passage of a cell through a microfluidic channel. We demonstrate that the rheology of the cell cytoplasm is important for capturing the transit time through a narrow channel in the presence of a pressure drop in the extracellular fluid.

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McGhee, Sean A., and Talal A. Chatila. "DOCK8 Immune Deficiency as a Model for Primary Cytoskeletal Dysfunction." Disease Markers 29, no. 3-4 (2010): 151–56. http://dx.doi.org/10.1155/2010/397291.

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DOCK8 deficiency is a newly described primary immune deficiency resulting in profound susceptibility to cutaneous viral infections, elevated IgE levels, and eosinophilia, but lacking in the skeletal manifestations commonly seen in hyper IgE syndrome, which it otherwise resembles. Although little is known about the DOCK8 protein, it resembles other atypical guanine exchange factors in the DOCK family, and is known to bind to CDC42. This suggests that a likely role for DOCK8 is in modulating signals that trigger cytoskeletal reorganization. As a result, DOCK8 may also be related to other immune deficiencies that involve the cytoskeleton and Rho GTPase signaling pathways, such as Wiskott-Aldrich syndrome and Rac2 deficiency.

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Ghaffari, Hamed, Mohammad Said Saidi, and Bahar Firoozabadi. "Biomechanical analysis of actin cytoskeleton function based on a spring network cell model." Proceedings of the Institution of Mechanical Engineers, Part C: Journal of Mechanical Engineering Science 231, no. 7 (October 3, 2016): 1308–23. http://dx.doi.org/10.1177/0954406216668546.

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In this study, a new method for the simulation of the time-dependent behavior of actin cytoskeleton during cell shape change is proposed. For this purpose, a three-dimensional model of endothelial cell consisting of cell membrane, nucleus membrane, and main components of cytoskeleton, namely actin filaments, microtubules, and intermediate filaments is utilized. Actin binding proteins, which play a key role in regulating actin cytoskeleton behavior, are also simulated by using a novel technique. The actin cytoskeleton in this model is more dynamic and adoptable during cell deformation in comparison to previous models. The proposed model is subjected to compressive force between parallel micro plates in order to investigate actin cytoskeleton role in cell stiffening behavior, nucleus deformation, and cell shape change. The validity of the model is examined through the comparison of the obtained results with the data presented in previous literature. Not only does the model force deformation curve lie within a range of the experimental data, but also the elastic modulus of the cell model is in accordance with former studies. Our findings demonstrate that augmentation of actin filaments concentration within the cell reduces force transmission from cell membrane to the nucleus. Furthermore, actin binding proteins concentration increases by the enhancement of cell deformation and it is also indicated that cell stiffening with an increase in applied force is significantly affected by actin filaments reorientation, actin binding proteins reorganization and actin binding proteins augmentation.

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Fostinis, Yannis, Panayotis A. Theodoropoulos, Achille Gravanis, and Christos Stournaras. "Heat shock protein HSP90 and its association with the cytoskeleton: a morphological study." Biochemistry and Cell Biology 70, no. 9 (September 1, 1992): 779–86. http://dx.doi.org/10.1139/o92-118.

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To investigate the cellular localization of the 90-kilodalton heat shock protein (HSP90) and its interaction with the cytoskeleton, we performed single- and double-staining immunofluorescence microscopy of cytoskeletal proteins and HSP90 in the absence and presence of cytoskeletal inhibitors. As a model, we used a human endometrial adenocarcinoma cell line (Ishikawa cells), which expresses HSP90. We confirmed the recently reported colocalization of HSP90 with microtubules. However, Ishikawa cells treated with 10−5 M of the antimicrotubule agents colchicine or triethyl lead showed residual filamentous structures stained with anti-HSP90 antibodies, while no microtubules were visualized with anti-tubulin antibodies. In the presence of 10−5 M cytochalasin B, the microfilament staining of the cells disappeared, while residual filamentous structures were labeled with anti-HSP90 antibodies. Furthermore, Ishikawa cells treated with 10−5 M triethyl lead and stained with anti-HSP90 antibodies demonstrated residual filamentous structures, clearly different from those of reorganized vimentin intermediate filaments. Conversely, similar reorganized morphology of filamentous structures stained with both anti-HSP90 and anti-cytokeratins antibodies were observed when Ishikawa cells were treated with 2 × 10−5 M cytochalasin B and 2 × 10−5 M colchicine. HSP90 was also present in Ishikawa cell preparations of the Triton X-100 insoluble cytoskeleton. In addition, Triton-insoluble cytoskeleton treated with 10−5 M triethyl lead and double stained with anti-HSP90 and anti-vimentin antibodies demonstrated clearly different filamentous patterns, when exposed on the same photographic plaque. However, after combined treatment of those preparations with 2 × 10−5 M cytochalasin B and 2 × 10−5 M colchicine, the filamentous structures double labeled with anti-HSP90 and anti-cytokeratins antibodies appeared to be similarly reorganized, showing comparable rearrangement characteristics, the later suggesting a possible association of HSP90 with keratin cytoskeleton. It is important to note that there is no in vitro cross-reaction of anti-HSP90 antibodies with any of the studied cytoskeletal proteins in Western blotting analysis.Key words: heat shock protein HSP90, cytoskeleton, immunofluorescence microscopy.

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Barns, Sarah, Emilie Sauret, Suvash Saha, Robert Flower, and Yuan Tong Gu. "Two-Layer Red Blood Cell Membrane Model Using the Discrete Element Method." Applied Mechanics and Materials 846 (July 2016): 270–75. http://dx.doi.org/10.4028/www.scientific.net/amm.846.270.

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The red blood cell (RBC) membrane consists of a lipid bilayer and spectrin-based cytoskeleton, which enclose haemoglobin-rich fluid. Numerical models of RBCs typically integrate the two membrane components into a single layer, preventing investigation of bilayer-cytoskeleton interaction. To address this constraint, a new RBC model which considers the bilayer and cytoskeleton separately is developed using the discrete element method (DEM). This is completed in 2D as a proof-of-concept, with an extension to 3D planned in the future. Resting RBC morphology predicted by the two-layer model is compared to an equivalent and well-established composite (one-layer) model with excellent agreement for critical cell dimensions. A parametric study is performed where area reduction ratio and spring constants are varied. It is found that predicted resting geometry is relatively insensitive to changes in spring stiffness, but a shape variation is observed for reduction ratio changes as expected.

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Guma, Fatima C. R., Tanira G. Mello, Claudia S. Mermelstein, Vitor A. Fortuna, Susana T. Wofchuk, Carmem Gottfried, Regina M. Guaragna, Manoel L. Costa, and Radovan Borojevic. "Intermediate filaments modulation in an in vitro model of the hepatic stellate cell activation or conversion into the lipocyte phenotype." Biochemistry and Cell Biology 79, no. 4 (August 1, 2001): 409–17. http://dx.doi.org/10.1139/o01-027.

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Hepatic stellate cells are intralobular connective tissue cells expressing the myofibroblast or the lipocyte phenotypes. They participate in homeostasis of the liver extracellular matrix, repair, regeneration, and fibrosis under the former phenotype, and control the retinol metabolism, storage, and release under the latter one. They are heterogeneous in terms of their tissue distribution, function, and expression of cytoskeletal proteins. We have studied the expressions of intermediate filaments in the cloned GRX cell line representative of murine hepatic stellate cells, by immunolabeling, reverse transcription polymerase chain reaction (RT-PCR), immunoprecipitation and Western blots. GRX cells expressed vimentin, desmin, glial fibrillary acidic protein (GFAP), and smooth muscle α actin (SM-αA). Vimentin, desmin, and SM-αA were expressed in all cultures. GFAP showed a heterogeneous intensity of expression and did not form a filamentous cytoskeletal network, showing a distinct punctuate cytoplasmic distribution. When activated by inflammatory mediators, GRX cells increased expression of desmin and GFAP. Retinol-mediated induction of the lipocyte phenotype elicited a strong decrease of intermediate filament protein expression and the collapse of the filamentous structure of the cytoskeleton. Quiescent hepatic stellate precursors can respond to physiologic or pathologic stimuli, expressing activated myofibroblast or lipocyte phenotypes with distinct patterns of cytoskeleton structure, metabolic function, and interaction with the tissue environment.Key words: intermediate filaments, desmin, glial fibrillary acidic protein, GFAP, hepatic stellate cells, liver.

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Bottazzi, Maria Elena, Monica Buzzai, Xiaoyun Zhu, Chantal Desdouets, Christian Bréchot, and Richard K. Assoian. "Distinct Effects of Mitogens and the Actin Cytoskeleton on CREB and Pocket Protein Phosphorylation Control the Extent and Timing of Cyclin A Promoter Activity." Molecular and Cellular Biology 21, no. 22 (November 15, 2001): 7607–16. http://dx.doi.org/10.1128/mcb.21.22.7607-7616.2001.

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ABSTRACT Soluble mitogens and adhesion-dependent organization of the actin cytoskeleton are required for cells to enter S phase in fibroblasts. The induction of cyclin A is also required for S-phase entry, and we now report that distinct effects of mitogens and the actin cytoskeleton on the phosphorylation of CREB and pocket proteins regulate the extent and timing of cyclin A promoter activity, respectively. First, we show that CREB phosphorylation and binding to the cyclic AMP response element (CRE) determines the extent, but not the timing, of cyclin A promoter activity. Second, we show that pocket protein inactivation regulates the timing, but not the extent, of cyclin A promoter activity. CREB phosphorylation and CRE occupancy are regulated by soluble mitogens alone, while the phosphorylation of pocket proteins requires both mitogens and the organized actin cytoskeleton. Mechanistically, cytoskeletal integrity controls pocket protein phosphorylation by allowing for sustained ERK signaling and, thereby, the expression of cyclin D1. Our results lead to a model of cyclin A gene regulation in which mitogens play a permissive role by stimulating early G1-phase phosphorylation of CREB and a distinct regulatory role by cooperating with the organized actin cytoskeleton to regulate the duration of ERK signaling, the expression of cyclin D1, and the timing of pocket protein phosphorylation.

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Liu, G., and P. C. Newell. "Evidence of cyclic GMP may regulate the association of myosin II heavy chain with the cytoskeleton by inhibiting its phosphorylation." Journal of Cell Science 98, no. 4 (April 1, 1991): 483–90. http://dx.doi.org/10.1242/jcs.98.4.483.

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Previous studies have implicated cyclic GMP in the regulation of myosin II heavy chain (MHC) association with the cytoskeleton in Dictyostelium discoideum. Here we provide evidence that cyclic GMP may regulate MHC association with the cytoskeleton through MHC phosphorylation. Comparative data are presented of MHC phosphorylation in the wild-type strain NC4, the parental strain XP55 and streamer mutants NP368 and NP377. Using an anti-MHC monoclonal antibody to immunoprecipitate MHC from [32P]phosphate-labelled developing cells, we found that cyclic AMP stimulation of the wild-type strain NC4 and parental strain XP55 induced MHC phosphorylation in vivo. A peak of phosphorylation was observed at 30–40 s, followed by a gradual decrease to basal level at 160 s. In contrast, in both of the streamer mutants NP368 and NP377 (which have prolonged cyclic GMP accumulation and prolonged MHC association with the cytoskeleton), the phosphorylation of MHC was delayed and did not form a peak until 60–80 s after cyclic AMP stimulation. We also found that cytoskeletal MHC showed only minor phosphorylation, the majority of the phosphorylated MHC being found in the cytosol. We present a model to account for these results in which cyclic GMP regulates MHC association with the cytoskeleton by regulating the phosphorylation/dephosphorylation cycle of MHC in these cells.

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Myers, Kenneth A., Jerome B. Rattner, Nigel G. Shrive, and David A. Hart. "Hydrostatic pressure sensation in cells: integration into the tensegrity model." Biochemistry and Cell Biology 85, no. 5 (October 2007): 543–51. http://dx.doi.org/10.1139/o07-108.

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Hydrostatic pressure (HP) is a mechanical stimulus that has received relatively little attention in the field of the cell biology of mechanotransduction. Generalized models, such as the tensegrity model, do not provide a detailed explanation of how HP might be detected. This is significant, because HP is an important mechanical stimulus, directing cell behaviour in a variety of tissues, including cartilage, bone, airways, and the vasculature. HP sensitivity may also be an important factor in certain clinical situations, as well as under unique environmental conditions such as microgravity. While downstream cellular effects have been well characterized, the initial HP sensation mechanism remains unclear. In vitro evidence shows that HP affects cytoskeletal polymerization, an effect that may be crucial in triggering the cellular response. The balance between free monomers and cytoskeletal polymers is shifted by alterations in HP, which could initiate a cellular response by releasing and (or) activating cytoskeleton-associated proteins. This new model fits well with the basic tenets of the existing tensegrity model, including mechanisms in which cellular HP sensitivity could be tuned to accommodate variable levels of stress.

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Hagan, I. M. "The fission yeast microtubule cytoskeleton." Journal of Cell Science 111, no. 12 (June 15, 1998): 1603–12. http://dx.doi.org/10.1242/jcs.111.12.1603.

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The Schizosaccharomyces pombe genome sequencing project (http://www.sanger.ac.uk/Projects/S_pombe/) is nearly complete, and this is likely to generate interest in fission yeast as a model system beyond its traditional strongholds in the study of the cell cycle and sexual differentiation. In many fields S. pombe will offer a useful complement to the more widely studied Saccharomyces cerevisiae, but in some areas the impact of S. pombe may well rival or exceed that of this budding yeast in terms of relevance to higher systems. Because of the considerable differences from the S. cerevisiae microtubule cytoskeleton, studying microtubules in S. pombe is likely to enhance the contribution of model systems to our understanding of the principles and practices of microtubule organisation in eukaryotes in general.

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Oliver-Gonzalez, Rubén, Carlos García-Tovar, Lourdes Juárez-Mosqueda, and Fernando Navarro-Garcia. "Infection of rabbit kidney cells (RK13) by enteropathogenicEscherichia colias a model to study the dynamics of actin cytoskeleton." Canadian Journal of Microbiology 54, no. 9 (September 2008): 748–57. http://dx.doi.org/10.1139/w08-069.

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Enteropathogenic Escherichia coli (EPEC) colonizes the intestinal mucosa and causes a cell lesion known as attachment and effacement (A/E) lesion. The molecular mechanisms for A/E lesions include injection of Tir, which is a receptor for an adhesin named intimin. The Tir–intimin interaction causes rearrangement of the cytoskeleton forming actin-rich structures called pedestals. Unfortunately, the formation of the A/E lesions and the dynamics of the actin cytoskeleton during this rearrangement induced by EPEC cannot be studied in the natural host. However, there are EPEC strains that infect rabbit (REPEC) that are genetically and pathologically similar to EPEC. Here, we used REPEC for the infection of rabbit kidney epithelial cells, line RK13, as a model to understand the actin cytoskeleton dynamics during pedestal formation. Actin-rich pedestal formation during the infection of RK13 cells by REPEC was analyzed by electron and confocal microscopy. The kinetics of infection along with the use of antibiotics for eliminating the bacteria, as well as reinfection, evidenced the plasticity of the actin cytoskeleton during pedestal formation. Thus, this model is a helpful tool for studying the dynamics of actin cytoskeleton and for correlating the data with those observed in in vivo models in rabbits experimentally infected with REPEC.

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Ganusova, Elena E., Laura N. Ozolins, Srishti Bhagat, Gary P. Newnam, Renee D. Wegrzyn, Michael Y. Sherman, and Yury O. Chernoff. "Modulation of Prion Formation, Aggregation, and Toxicity by the Actin Cytoskeleton in Yeast." Molecular and Cellular Biology 26, no. 2 (January 15, 2006): 617–29. http://dx.doi.org/10.1128/mcb.26.2.617-629.2006.

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ABSTRACT Self-perpetuating protein aggregates transmit prion diseases in mammals and heritable traits in yeast. De novo prion formation can be induced by transient overproduction of the corresponding prion-forming protein or its prion domain. Here, we demonstrate that the yeast prion protein Sup35 interacts with various proteins of the actin cortical cytoskeleton that are involved in endocytosis. Sup35-derived aggregates, generated in the process of prion induction, are associated with the components of the endocytic/vacuolar pathway. Mutational alterations of the cortical actin cytoskeleton decrease aggregation of overproduced Sup35 and de novo prion induction and increase prion-related toxicity in yeast. Deletion of the gene coding for the actin assembly protein Sla2 is lethal in cells containing the prion isoforms of both Sup35 and Rnq1 proteins simultaneously. Our data are consistent with a model in which cytoskeletal structures provide a scaffold for generation of large aggregates, resembling mammalian aggresomes. These aggregates promote prion formation. Moreover, it appears that the actin cytoskeleton also plays a certain role in counteracting the toxicity of the overproduced potentially aggregating proteins.

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Tan, Minghui, Caihui Cha, Yongheng Ye, Jifeng Zhang, Sumei Li, Fengming Wu, Sitang Gong, and Guoqing Guo. "CRMP4 and CRMP2 Interact to Coordinate Cytoskeleton Dynamics, Regulating Growth Cone Development and Axon Elongation." Neural Plasticity 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/947423.

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Cytoskeleton dynamics are critical phenomena that underpin many fundamental cellular processes. Collapsin response mediator proteins (CRMPs) are highly expressed in the developing nervous system, mediating growth cone guidance, neuronal polarity, and axonal elongation. However, whether and how CRMPs associate with microtubules and actin coordinated cytoskeletal dynamics remain unknown. In this study, we demonstrated that CRMP2 and CRMP4 interacted with tubulin and actinin vitroand colocalized with the cytoskeleton in the transition-zone in developing growth cones. CRMP2 and CRMP4 also interacted with one another coordinately to promote growth cone development and axonal elongation. Genetic silencing of CRMP2 enhanced, whereas overexpression of CRMP2 suppressed, the inhibitory effects of CRMP4 knockdown on axonal development. In addition, knockdown of CRMP2 or overexpression of truncated CRMP2 reversed the promoting effect of CRMP4. With the overexpression of truncated CRMP2 or CRMP4 lacking the cytoskeleton interaction domain, the promoting effect of CRMP was suppressed. These data suggest a model in which CRMP2 and CRMP4 form complexes to bridge microtubules and actin and thus work cooperatively to regulate growth cone development and axonal elongation.

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Thuillier, Raphael, and Thierry Hauet. "Impact of Hypothermia and Oxygen Deprivation on the Cytoskeleton in Organ Preservation Models." BioMed Research International 2018 (July 16, 2018): 1–10. http://dx.doi.org/10.1155/2018/8926724.

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Ischemia reperfusion (IR) lesions are an unavoidable consequence of organ transplantation. Researching new therapeutics against these lesions requires the definition of early mechanisms. The cytoskeleton is composed of 3 types of filaments: microfilaments, intermediate filaments, and microtubules. We aimed to characterize the influence of preservation on their phenotype. In an in vitro model using primary human endothelial cells reproducing the conditions of organ preservation, two aspects were explored: (a) the impact of IR and cold ischemia time on each filament type, evaluating the roles of temperature, solution, and oxygen; and (b) the potential of cytoskeleton-mediated therapy to alleviate cell death. Results showed that intermediary filaments were unaffected, while microfilaments showed radical changes with disappearance of the structure replaced by a disorganized array of nodules; moreover, microtubules almost completely disappeared with time. Furthermore, temperature, and not oxygen deprivation or the solution, was the determining factor of the cytoskeleton’s loss of integrity during preservation. Finally, pharmaceutical intervention could indeed preserve fiber structure but did not alter survival. Our work shows that improvement of preservation must include a more adapted temperature before considering oxygen, as it could profoundly improve cytoskeleton organization and thus cell fate. This highlights the importance of this structure for the development of new therapeutics and the definition of graft quality biomarkers.

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Cañadas, Patrick, Bernard Maurin, Haimad Baudriller, Philippe Montcourrier, and Nadir Bettache. "NUMERICAL MODEL OF THE CYTOSKELETON STRUCTURATION DURING CELL SPREADING." Journal of Biomechanics 41 (July 2008): S20. http://dx.doi.org/10.1016/s0021-9290(08)70020-4.

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Hart, T. N., and L. E. H. Trainor. "The two-component model for the cytoskeleton in development." Physica D: Nonlinear Phenomena 44, no. 3 (September 1990): 269–84. http://dx.doi.org/10.1016/0167-2789(90)90149-j.

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Mao, Bai-Ping, Linxi Li, Ming Yan, Renshan Ge, Qingquan Lian, and C. Yan Cheng. "Regulation of BTB Dynamics in Spermatogenesis—Insights From the Adjudin Model." Toxicological Sciences 172, no. 1 (August 9, 2019): 75–88. http://dx.doi.org/10.1093/toxsci/kfz180.

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Abstract During spermatogenesis, cell organelles, and germ cells, most notably haploid spermatids, are transported across the seminiferous epithelium so that fully developed spermatids line-up at the edge of the tubule lumen to undergo spermiation at stage VIII of the cycle. Studies have suggested that the microtubule (MT)-based cytoskeleton is necessary to support these cellular events. However, the regulatory molecule(s) and underlying mechanism(s) remain poorly understood. Herein, we sought to better understand this event by using an adjudin-based animal model. Adult rats were treated with adjudin at low-dose (10 mg/kg b.w.) which by itself had no notable effects on spermatogenesis. Rats were also treated with low-dose adjudin combined with overexpression of 2 endogenously produced blood-testis barrier (BTB) modifiers, namely rpS6 (ribosomal protein S6, the downstream signaling protein of mammalian target of rapamycin complex 1 [mTORC1]) and F5-peptide (a biological active peptide released from laminin-γ3 chain at the Sertoli-spermatid interface) versus the 2 BTB modifiers alone. Overexpression of these 2 BTB modifiers in the testis was shown to enhance delivery of adjudin to the testis, effectively inducing disruptive changes in MT cytoskeletons, causing truncation of MT conferred tracks that led to their collapse across the epithelium. The net result was massive germ cell exfoliation in the tubules, disrupting germ cell transport and cell adhesion across the seminiferous epithelium that led to aspermatogenesis. These changes were the result of disruptive spatial expression of several MT-based regulatory proteins. In summary, MT cytoskeleton supported by the network of MT regulatory proteins is crucial to maintain spermatogenesis.

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Bhatnagar, Rajendra S., Steven B. Nicoll, Jing Jing Qian, and Nancy Smith. "A Tissue Engineering Model for Tractional Organization of Cells and Matrices." Microscopy and Microanalysis 7, S2 (August 2001): 122–23. http://dx.doi.org/10.1017/s1431927600026684.

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Tissues are characterized by highly distinctive microarchitecture and overall form that are critical to tissue specific function. with increasing interest in tissue engineering to create surrogates for human tissues and organs, innovative techniques have been developed to generate scaffolds that display form, and microarchitecture mimicking physiological structures. While this artifice may generate pre-programmed shapes, it fails to take advantage of the inherent ability of cells to organize themselves and their surroundings. The generation of mechanical forces by the cellular cytoskeleton plays a critical role in the organization of matrix and of cellular colonies. The anchorage of the cytoskeleton to a substrate is essential for cellular tractional processes. in tissues, cells are anchored in a stationary, 3-D network of collagen in a highly characteristic spatial arrangement. This spatial order arises from vectorial deposition of matrix and its subsequent tractional organization by cells. The junction of the cell binding domain of collagen with specific integrin receptors, and the cells’ cytoskeleton comprises the apparatus for the interconversion of mechanical and biochemical energy.

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Breuer, David, Alexander Ivakov, Arun Sampathkumar, Florian Hollandt, Staffan Persson, and Zoran Nikoloski. "Quantitative analyses of the plant cytoskeleton reveal underlying organizational principles." Journal of The Royal Society Interface 11, no. 97 (August 6, 2014): 20140362. http://dx.doi.org/10.1098/rsif.2014.0362.

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The actin and microtubule (MT) cytoskeletons are vital structures for cell growth and development across all species. While individual molecular mechanisms underpinning actin and MT dynamics have been intensively studied, principles that govern the cytoskeleton organization remain largely unexplored. Here, we captured biologically relevant characteristics of the plant cytoskeleton through a network-driven imaging-based approach allowing us to quantitatively assess dynamic features of the cytoskeleton. By introducing suitable null models, we demonstrate that the plant cytoskeletal networks exhibit properties required for efficient transport, namely, short average path lengths and high robustness. We further show that these advantageous features are maintained during temporal cytoskeletal rearrangements. Interestingly, man-made transportation networks exhibit similar properties, suggesting general laws of network organization supporting diverse transport processes. The proposed network-driven analysis can be readily used to identify organizational principles of cytoskeletons in other organisms.

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Pathak, Amit, Vikram S. Deshpande, Robert M. McMeeking, and Anthony G. Evans. "The simulation of stress fibre and focal adhesion development in cells on patterned substrates." Journal of The Royal Society Interface 5, no. 22 (October 16, 2007): 507–24. http://dx.doi.org/10.1098/rsif.2007.1182.

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The remodelling of the cytoskeleton and focal adhesion (FA) distributions for cells on substrates with micro-patterned ligand patches is investigated using a bio-chemo-mechanical model. We investigate the effect of ligand pattern shape on the cytoskeletal arrangements and FA distributions for cells having approximately the same area. The cytoskeleton model accounts for the dynamic rearrangement of the actin/myosin stress fibres. It entails the highly nonlinear interactions between signalling, the kinetics of tension-dependent stress-fibre formation/dissolution and stress-dependent contractility. This model is coupled with another model that governs FA formation and accounts for the mechano-sensitivity of the adhesions from thermodynamic considerations. This coupled modelling scheme is shown to capture a variety of key experimental observations including: (i) the formation of high concentrations of stress fibres and FAs at the periphery of circular and triangular, convex-shaped ligand patterns; (ii) the development of high FA concentrations along the edges of the V-, T-, Y- and U-shaped concave ligand patterns; and (iii) the formation of highly aligned stress fibres along the non-adhered edges of cells on the concave ligand patterns. When appropriately calibrated, the model also accurately predicts the radii of curvature of the non-adhered edges of cells on the concave-shaped ligand patterns.

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Saito, Fumiyasu, Yohsuke Imai, Shunichi Ishida, Toshihiro Omori, and Takuji Ishikawa. "PS3-7 DEVELOPMENT OF A NUMERICAL MODEL OF CYTOSKELETON DYNAMICS(PS3: Poster Short Presentation III,Poster Session)." Proceedings of the Asian Pacific Conference on Biomechanics : emerging science and technology in biomechanics 2015.8 (2015): 268. http://dx.doi.org/10.1299/jsmeapbio.2015.8.268.

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Loiseau, Etienne, Jochen A. M. Schneider, Felix C. Keber, Carina Pelzl, Gladys Massiera, Guillaume Salbreux, and Andreas R. Bausch. "Shape remodeling and blebbing of active cytoskeletal vesicles." Science Advances 2, no. 4 (April 2016): e1500465. http://dx.doi.org/10.1126/sciadv.1500465.

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Morphological transformations of living cells, such as shape adaptation to external stimuli, blebbing, invagination, or tethering, result from an intricate interplay between the plasma membrane and its underlying cytoskeleton, where molecular motors generate forces. Cellular complexity defies a clear identification of the competing processes that lead to such a rich phenomenology. In a synthetic biology approach, designing a cell-like model assembled from a minimal set of purified building blocks would allow the control of all relevant parameters. We reconstruct actomyosin vesicles in which the coupling of the cytoskeleton to the membrane, the topology of the cytoskeletal network, and the contractile activity can all be precisely controlled and tuned. We demonstrate that tension generation of an encapsulated active actomyosin network suffices for global shape transformation of cell-sized lipid vesicles, which are reminiscent of morphological adaptations in living cells. The observed polymorphism of our cell-like model, such as blebbing, tether extrusion, or faceted shapes, can be qualitatively explained by the protein concentration dependencies and a force balance, taking into account the membrane tension, the density of anchoring points between the membrane and the actin network, and the forces exerted by molecular motors in the actin network. The identification of the physical mechanisms for shape transformations of active cytoskeletal vesicles sets a conceptual and quantitative benchmark for the further exploration of the adaptation mechanisms of cells.

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Alisafaei, Farid, Doorgesh Sharma Jokhun, G. V. Shivashankar, and Vivek B. Shenoy. "Regulation of nuclear architecture, mechanics, and nucleocytoplasmic shuttling of epigenetic factors by cell geometric constraints." Proceedings of the National Academy of Sciences 116, no. 27 (June 17, 2019): 13200–13209. http://dx.doi.org/10.1073/pnas.1902035116.

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Cells sense mechanical signals from their microenvironment and transduce them to the nucleus to regulate gene expression programs. To elucidate the physical mechanisms involved in this regulation, we developed an active 3D chemomechanical model to describe the three-way feedback between the adhesions, the cytoskeleton, and the nucleus. The model shows local tensile stresses generated at the interface of the cell and the extracellular matrix regulate the properties of the nucleus, including nuclear morphology, levels of lamin A,C, and histone deacetylation, as these tensile stresses 1) are transmitted to the nucleus through cytoskeletal physical links and 2) trigger an actomyosin-dependent shuttling of epigenetic factors. We then show how cell geometric constraints affect the local tensile stresses and subsequently the three-way feedback and induce cytoskeleton-mediated alterations in the properties of the nucleus such as nuclear lamina softening, chromatin stiffening, nuclear lamina invaginations, increase in nuclear height, and shrinkage of nuclear volume. We predict a phase diagram that describes how the disruption of cytoskeletal components impacts the feedback and subsequently induce contractility-dependent alterations in the properties of the nucleus. Our simulations show that these changes in contractility levels can be also used as predictors of nucleocytoplasmic shuttling of transcription factors and the level of chromatin condensation. The predictions are experimentally validated by studying the properties of nuclei of fibroblasts on micropatterned substrates with different shapes and areas.

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Al-Mamun, Mohammed, Lorna Ravenhill, Worawut Srisukkham, Alamgir Hossain, Charles Fall, Vincent Ellis, and Rosemary Bass. "Effects of Noninhibitory Serpin Maspin on the Actin Cytoskeleton: A Quantitative Image Modeling Approach." Microscopy and Microanalysis 22, no. 2 (February 24, 2016): 394–409. http://dx.doi.org/10.1017/s1431927616000520.

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AbstractRecent developments in quantitative image analysis allow us to interrogate confocal microscopy images to answer biological questions. Clumped and layered cell nuclei and cytoplasm in confocal images challenges the ability to identify subcellular compartments. To date, there is no perfect image analysis method to identify cytoskeletal changes in confocal images. Here, we present a multidisciplinary study where an image analysis model was developed to allow quantitative measurements of changes in the cytoskeleton of cells with different maspin exposure. Maspin, a noninhibitory serpin influences cell migration, adhesion, invasion, proliferation, and apoptosis in ways that are consistent with its identification as a tumor metastasis suppressor. Using different cell types, we tested the hypothesis that reduction in cell migration by maspin would be reflected in the architecture of the actin cytoskeleton. A hybrid marker-controlled watershed segmentation technique was used to segment the nuclei, cytoplasm, and ruffling regions before measuring cytoskeletal changes. This was informed by immunohistochemical staining of cells transfected stably or transiently with maspin proteins, or with added bioactive peptides or protein. Image analysis results showed that the effects of maspin were mirrored by effects on cell architecture, in a way that could be described quantitatively.

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Keković, G., D. Raković, M. V. Satarić, and Dj Koruga. "A Kink-Soliton Model of Charge Transport through Microtubular Cytoskeleton." Materials Science Forum 494 (September 2005): 507–12. http://dx.doi.org/10.4028/www.scientific.net/msf.494.507.

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Contemporary trends in science and technology are characterized by integration of biological and technical systems, like in nanotechnology, nanobiology, and quantum medicine. In our case, we were motivated by a necessity to understand charge transport through microtubular cytoskeleton as a constitutive part of acupuncture system. The high frequency component of acupuncture currents, widely exploited in microwave resonance stimulation of acupuncture system in the past decade, implies that explanation of the cytoplasmatic conductivity should be sought in the framework of Frohlich theory. Accordingly, in this paper we critically analyze the problem of the microwave coherent longitudinal electrical oscillations as a theoretical basis for understanding soliton phenomena in microtubules, showing that charged kink-soliton nonlinear microtubular excitations might be a good candidate for charge transport in microtubules.

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Coughlin, Mark F., and Dimitrije Stamenović. "A Prestressed Cable Network Model of the Adherent Cell Cytoskeleton." Biophysical Journal 84, no. 2 (February 2003): 1328–36. http://dx.doi.org/10.1016/s0006-3495(03)74948-0.

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Boal, D. H. "Computer simulation of a model network for the erythrocyte cytoskeleton." Biophysical Journal 67, no. 2 (August 1994): 521–29. http://dx.doi.org/10.1016/s0006-3495(94)80511-9.

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Gong, Jinghai, Daxu Zhang, Yiider Tseng, Baolong Li, Denis Wirtz, and Benjamin William Schafer. "Form-Finding Model Shows How Cytoskeleton Network Stiffness Is Realized." PLoS ONE 8, no. 10 (October 17, 2013): e77417. http://dx.doi.org/10.1371/journal.pone.0077417.

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Wang, Shenshen, and Peter G. Wolynes. "Tensegrity and motor-driven effective interactions in a model cytoskeleton." Journal of Chemical Physics 136, no. 14 (April 14, 2012): 145102. http://dx.doi.org/10.1063/1.3702583.

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LEE, David, Kikuo KISHIMOTO, Tadaharu ADACHI, and Atsushi IKAI. "749 A Network Model of Active Processes in the Cytoskeleton." Proceedings of The Computational Mechanics Conference 2008.21 (2008): 862–63. http://dx.doi.org/10.1299/jsmecmd.2008.21.862.

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Inoue, Yasuhiro, Taiji Adachi, and Masaki Hojo. "2010 Thermodynamic model of mechanoresponsive binding of cytoskeleton-regulatory proteins." Proceedings of The Computational Mechanics Conference 2009.22 (2009): 761–62. http://dx.doi.org/10.1299/jsmecmd.2009.22.761.

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Campillo, Clément, Léa-Laetitia Pontani, Pierre Nassoy, Patricia Bassereau, and Cécile Sykes. "Nanotether Extrusion to probe Membrane-Cytoskeleton Interaction in Model Systems." Biophysical Journal 96, no. 3 (February 2009): 386a. http://dx.doi.org/10.1016/j.bpj.2008.12.2891.

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Fan, Houfu, and Shaofan Li. "Modeling microtubule cytoskeleton via an active liquid crystal elastomer model." Computational Materials Science 96 (January 2015): 559–66. http://dx.doi.org/10.1016/j.commatsci.2014.04.041.

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Maurin, B., P. Cañadas, H. Baudriller, P. Montcourrier, and N. Bettache. "Mechanical model of cytoskeleton structuration during cell adhesion and spreading." Journal of Biomechanics 41, no. 9 (January 2008): 2036–41. http://dx.doi.org/10.1016/j.jbiomech.2008.03.011.

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Loosli, Y., R. Luginbuehl, and J. G. Snedeker. "Cytoskeleton reorganization of spreading cells on micro-patterned islands: a functional model." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 368, no. 1920 (June 13, 2010): 2629–52. http://dx.doi.org/10.1098/rsta.2010.0069.

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Predictive numerical models of cellular response to biophysical cues have emerged as a useful quantitative tool for cell biology research. Cellular experiments in silico can augment in vitro and in vivo investigations by filling gaps in what is possible to achieve through ‘wet work’. Biophysics-based numerical models can be used to verify the plausibility of mechanisms regulating tissue homeostasis derived from experiments. They can also be used to explore potential targets for therapeutic intervention. In this perspective article we introduce a single cell model developed towards the design of novel biomaterials to elicit a regenerative cellular response for the repair of diseased tissues. The model is governed by basic mechanisms of cell spreading (lamellipodial and filopodial extension, formation of cell–matrix adhesions, actin reinforcement) and is developed in the context of cellular interaction with functionalized substrates that present defined points of potential adhesion. To provide adequate context, we first review the biophysical underpinnings of the model as well as reviewing existing cell spreading models. We then present preliminary benchmarking of the model against published experiments of cell spreading on micro-patterned substrates. Initial results indicate that our mechanistic model may represent a potentially useful approach in a better understanding of cell interactions with the extracellular matrix.

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Journal articles on the topic 'Cytoskeleton model'

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