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Journal articles on the topic 'Substrate rigidity'

Author: Grafiati

Published: 25 May 2024

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1

Wang, Hong-Bei, Micah Dembo, and Yu-Li Wang. "Substrate flexibility regulates growth and apoptosis of normal but not transformed cells." American Journal of Physiology-Cell Physiology 279, no. 5 (November 1, 2000): C1345—C1350. http://dx.doi.org/10.1152/ajpcell.2000.279.5.c1345.

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One of the hallmarks of oncogenic transformation is anchorage-independent growth (27). Here we demonstrate that responses to substrate rigidity play a major role in distinguishing the growth behavior of normal cells from that of transformed cells. We cultured normal or H- ras-transformed NIH 3T3 cells on flexible collagen-coated polyacrylamide substrates with similar chemical properties but different rigidity. Compared with cells cultured on stiff substrates, nontransformed cells on flexible substrates showed a decrease in the rate of DNA synthesis and an increase in the rate of apoptosis. These responses on flexible substrates are coupled to decreases in cell spreading area and traction forces. In contrast, transformed cells maintained their growth and apoptotic characteristics regardless of substrate flexibility. The responses in cell spreading area and traction forces to substrate flexibility were similarly diminished. Our results suggest that normal cells are capable of probing substrate rigidity and that proper mechanical feedback is required for regulating cell shape, cell growth, and survival. The loss of this response can explain the unregulated growth of transformed cells.

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2

Doss, Bryant L., Meng Pan, Mukund Gupta, Gianluca Grenci, René-Marc Mège, Chwee Teck Lim, Michael P. Sheetz, Raphaël Voituriez, and Benoît Ladoux. "Cell response to substrate rigidity is regulated by active and passive cytoskeletal stress." Proceedings of the National Academy of Sciences 117, no. 23 (May 22, 2020): 12817–25. http://dx.doi.org/10.1073/pnas.1917555117.

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Morphogenesis, tumor formation, and wound healing are regulated by tissue rigidity. Focal adhesion behavior is locally regulated by stiffness; however, how cells globally adapt, detect, and respond to rigidity remains unknown. Here, we studied the interplay between the rheological properties of the cytoskeleton and matrix rigidity. We seeded fibroblasts onto flexible microfabricated pillar arrays with varying stiffness and simultaneously measured the cytoskeleton organization, traction forces, and cell-rigidity responses at both the adhesion and cell scale. Cells adopted a rigidity-dependent phenotype whereby the actin cytoskeleton polarized on stiff substrates but not on soft. We further showed a crucial role of active and passive cross-linkers in rigidity-sensing responses. By reducing myosin II activity or knocking down α-actinin, we found that both promoted cell polarization on soft substrates, whereas α-actinin overexpression prevented polarization on stiff substrates. Atomic force microscopy indentation experiments showed that this polarization response correlated with cell stiffness, whereby cell stiffness decreased when active or passive cross-linking was reduced and softer cells polarized on softer matrices. Theoretical modeling of the actin network as an active gel suggests that adaptation to matrix rigidity is controlled by internal mechanical properties of the cytoskeleton and puts forward a universal scaling between nematic order of the actin cytoskeleton and the substrate-to-cell elastic modulus ratio. Altogether, our study demonstrates the implication of cell-scale mechanosensing through the internal stress within the actomyosin cytoskeleton and its coupling with local rigidity sensing at focal adhesions in the regulation of cell shape changes and polarity.

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3

O'Connor, Roddy, Xueli Hao, Keyue Shen, Keenan Bashour, Lance Kam, and Michael Milone. "Substrate rigidity regulates human T cell activation and proliferation (52.9)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 52.9. http://dx.doi.org/10.4049/jimmunol.188.supp.52.9.

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Abstract Adoptive immunotherapy using cultured T cells holds promise for the treatment of cancer and infectious disease. Culture platforms based upon hard materials, such as polystyrene plastic, form the basis of many culture systems. The mechanical properties of a culture substrate can influence cellular adhesion, proliferation, and differentiation. We explored the impact of substrate stiffness on ex vivo T cell activation and polyclonal expansion using substrates with variable rigidity manufactured from poly(dimethylsiloxane) (PDMS), a biocompatible silicone elastomer. We show that the IL-2 production and ex vivo proliferation of human CD4+ and CD8+ T cells are increased an average of 4-fold following stimulation on softer (Young’s Modulus [E] < 100 kPa) compared with stiffer (E >2 MPa) substrates. Mixed peripheral blood T cells cultured on the stiffer substrates also demonstrate a trend towards a greater proportion of CD62Lneg, effector-differentiated CD4+ and CD8+ T cells. Culture of naïve CD4+ T cells on softer substrates yields an average 3-fold greater proportion of IFN-γ producing TH1-like cells. These findings reveal that the rigidity of the substrate used to immobilize T cell stimulatory ligands is an important and previously unrecognized parameter for T cell culture systems used for adoptive immunotherapy. These results also have implications for studies of T cell activation and signal transduction that use immobilized TCR/CD3 and CD28 ligands.

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4

Banerjee, S., and M. C. Marchetti. "Substrate rigidity deforms and polarizes active gels." EPL (Europhysics Letters) 96, no. 2 (September 28, 2011): 28003. http://dx.doi.org/10.1209/0295-5075/96/28003.

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5

York, B. R., S. A. Solin, N. Wada, Rasik H. Raythatha, Ivy D. Johnson, and Thomas J. Pinnavaia. "Substrate rigidity effects in mixed layered solids." Solid State Communications 54, no. 6 (May 1985): 475–78. http://dx.doi.org/10.1016/0038-1098(85)90650-7.

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6

Lovett, David B., Nandini Shekhar, Jeffrey A. Nickerson, Kyle J. Roux, and Tanmay P. Lele. "Modulation of Nuclear Shape by Substrate Rigidity." Cellular and Molecular Bioengineering 6, no. 2 (February 5, 2013): 230–38. http://dx.doi.org/10.1007/s12195-013-0270-2.

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7

Roberts, M. W., C. B. Clemons, J. P. Wilber, G. W. Young, A. Buldum, and D. D. Quinn. "Continuum Plate Theory and Atomistic Modeling to Find the Flexural Rigidity of a Graphene Sheet Interacting with a Substrate." Journal of Nanotechnology 2010 (2010): 1–8. http://dx.doi.org/10.1155/2010/868492.

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Using a combination of continuum modeling, atomistic simulations, and numerical optimization, we estimate the flexural rigidity of a graphene sheet. We consider a rectangular sheet that is initially parallel to a rigid substrate. The sheet interacts with the substrate by van der Waals forces and deflects in response to loading on a pair of opposite edges. To estimate the flexural rigidity, we model the graphene sheet as a continuum and numerically solve an appropriate differential equation for the transverse deflection. This solution depends on the flexural rigidity. We then use an optimization procedure to find the value of the flexural rigidity that minimizes the difference between the numerical solutions and the deflections predicted by atomistic simulations. This procedure predicts a flexural rigidity of 0.26 nNnm=1.62 eV.

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8

Gong, Ze, Spencer E. Szczesny, Steven R. Caliari, Elisabeth E. Charrier, Ovijit Chaudhuri, Xuan Cao, Yuan Lin, et al. "Matching material and cellular timescales maximizes cell spreading on viscoelastic substrates." Proceedings of the National Academy of Sciences 115, no. 12 (March 5, 2018): E2686—E2695. http://dx.doi.org/10.1073/pnas.1716620115.

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Recent evidence has shown that, in addition to rigidity, the viscous response of the extracellular matrix (ECM) significantly affects the behavior and function of cells. However, the mechanism behind such mechanosensitivity toward viscoelasticity remains unclear. In this study, we systematically examined the dynamics of motor clutches (i.e., focal adhesions) formed between the cell and a viscoelastic substrate using analytical methods and direct Monte Carlo simulation. Interestingly, we observe that, for low ECM rigidity, maximum cell spreading is achieved at an optimal level of viscosity in which the substrate relaxation time falls between the timescale for clutch binding and its characteristic binding lifetime. That is, viscosity serves to stiffen soft substrates on a timescale faster than the clutch off-rate, which enhances cell−ECM adhesion and cell spreading. On the other hand, for substrates that are stiff, our model predicts that viscosity will not influence cell spreading, since the bound clutches are saturated by the elevated stiffness. The model was tested and validated using experimental measurements on three different material systems and explained the different observed effects of viscosity on each substrate. By capturing the mechanism by which substrate viscoelasticity affects cell spreading across a wide range of material parameters, our analytical model provides a useful tool for designing biomaterials that optimize cellular adhesion and mechanosensing.

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9

Chaky, J., K. Anderson, M. Moss, and L. Vaillancourt. "Surface Hydrophobicity and Surface Rigidity Induce Spore Germination in Colletotrichum graminicola." Phytopathology® 91, no. 6 (June 2001): 558–64. http://dx.doi.org/10.1094/phyto.2001.91.6.558.

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We investigated the relationship between physical characteristics of artificial surfaces, spore attachment, and spore germination in Colletotrichum graminicola. Surface hydrophobicity and surface rigidity were both signals for breaking dormancy and initiating spore germination, but spore attachment alone was not an important inducing signal. The presence of a carbon source overrode the necessity for a rigid, hydrophobic substrate for spore germination. Spore attachment was typically stronger to more hydrophobic surfaces, but certain hydrophilic surfaces also proved to be good substrates for spore attachment. In contrast to spore germination, appressorial induction was more dependent on attachment to a rigid substrate than it was on surface hydrophobicity. Appressoria were induced efficiently on hydrophilic surfaces, as long as there was significant conidial attachment to those surfaces.

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10

Wang, ZQ, ZL Dan, and J. Wu. "A Simple Solution to the Cylindrical Indentation of an Elastic Compressible Thin Layer Resting on a Rigid Substrate." Journal of Physics: Conference Series 2095, no. 1 (November 1, 2021): 012094. http://dx.doi.org/10.1088/1742-6596/2095/1/012094.

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Abstract In this paper, an analytical model is presented to study the contact that recedes between an elastic thin film that could be compressed and a substrate of rigidity. The surface of rigidity was formed due to cylindrical indentation. The substrate was assumed to be a rough surface without any friction. Further, the contact width of the substrate was derived, and the relationship between the compression force, compression depth, and the compression width was determined using the energy method. Finally, the obtained results were validated using finite element analysis.

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11

Ni, Yong, and Martin Y. M. Chiang. "Cell morphology and migration linked to substrate rigidity." Soft Matter 3, no. 10 (2007): 1285. http://dx.doi.org/10.1039/b703376a.

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12

Boccafoschi, Francesca, Marco Rasponi, Cecilia Mosca, Erica Bocchi, and Simone Vesentini. "Study of Cellular Adhesion by Means of Micropillar Surface Topologies." Advanced Materials Research 409 (November 2011): 105–10. http://dx.doi.org/10.4028/www.scientific.net/amr.409.105.

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It is well-known that cellular behavior can be guided by chemical signals and physical interactions at the cell-substrate interface. The patterns that cells encounter in their natural environment include nanometer-to-micrometer-sized topographies comprising extracellular matrix, proteins, and adjacent cells. Whether cells transduce substrate rigidity at the microscopic scale (for example, sensing the rigidity between adhesion sites) or the nanoscopic scale remains an open question. Here we report that micromolded elastomeric micropost arrays can decouple substrate rigidity from adhesive and surface properties. Arrays of poly (dimethylsiloxane) (PDMS) microposts from microfabricated silicon masters have been fabricated. To control substrate rigidity they present the same post heights but different surface area and spacing between posts. The main advantage of micropost arrays over other surface modification solutions (i.e. hydrogels) is that measured subcellular traction forces could be attributed directly to focal adhesions. This would allow to map traction forces to individual focal adhesions and spatially quantify subcellular distributions of focal-adhesion area, traction force and focal-adhesion stress. Moreover, different adhesion intracellular pathways could be used by the cells to differentiate toward a proliferative or a contractile cellular phenotype, for instance. This particular application is advantageous for vascular tissue engineering applications, where mimicking as close as possible the vessels dynamics should be a step forward in this research field.

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13

Shi, Lingting, Jounghyun Helen Lee, and Lance Kam. "Substrate rigidity affects human regulatory T cell induction in vitro." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 128.18. http://dx.doi.org/10.4049/jimmunol.202.supp.128.18.

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Abstract Immunotherapy using regulatory T cells (Tregs) has shown recent successes in the treatment of autoimmune and inflammatory diseases such as type 1 diabetes. While natural Tregs are unstable and dysfunctional in the inflammatory milieu, induced Tregs are more potent and durable. Tregs can be induced from CD4+CD25− T cells in vitro with TGF-β and IL-2 during activation. Chemical pathways in Treg induction have been heavily investigated, but the impact of mechanical cues on Treg induction has not been thoroughly explored. As T cell activation has been shown to be sensitive to the rigidity of the activating substrate, Treg induction may also be modulated by substrate rigidity. To test this hypothesis, Tregs were induced with 10 ng/ml TGF-β and IL-2 on different rigidities of polyacrylamide gels (5 to 110 kPa) coated with anti-CD3 and anti-CD28. The hydrogel stiffness was controlled by adjusting the acrylamide monomer and crosslinker content. The density of activating antibodies was varied by altering the concentration of streptavidin acrylamide that allows the binding of biotinylated antibodies to the gels. High ligand density on the stiffer substrate significantly upregulated the rate of Treg induction, measured by percent Foxp3 high T cells. Decreasing the ligand density shifted the optimal rigidity to softer substrates. This preliminary data has shown that Treg induction is mechanosensitive and dependent on ligand density, which can contribute to the understanding of mechanosensing in Treg induction and the improvement of biomaterial design for generating functional and stable Tregs to advance Treg adoptive therapy.

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14

Sarvestami, Alireza, Madeline Smith, Arsha Moorthy, Patrick Kho, Lauren Talbo, and Chamaree de Silva. "Rigidity sensing by blood-borne leukocytes: Is it independent of internal signaling?" AIMS Biophysics 11, no. 1 (2024): 18–30. http://dx.doi.org/10.3934/biophy.2024002.

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<abstract> <p>Atherosclerosis is a chronic inflammatory disease that results in the formation of lipid-rich lesions and stiffening of arterial walls. An increasing body of evidence suggests that nearly all members of the leukocyte family accumulate within atherosclerosis-prone arteries and participate in various stages of disease progression. Recently, it has been proposed that progressive changes of the elastic modulus of the arterial wall during plaque development may directly influence the kinematics of leukocyte rolling. In the present study, we propose that rigidity sensing of rolling leukocytes may occur spontaneously due to the stiffness-dependent elastic instability of reversible bonds between rolling leukocytes and the arterial walls. This effect is mechanistic in nature and operates independently of cell biochemical signaling. To partially test this hypothesis, we measured the rolling velocities of functionalized microparticles, comparable in size to leukocytes, interacting with E-selectin coated substrates of controlled stiffness. The kinematic analysis of the particles' motion reveals a larger rolling velocity on softer substrates, aligning with previous reports regarding monocytes. A simple kinetic model for a cluster of reversible bonds formed between a cell and the underlying substrate demonstrates that the critical forces needed for bond disassembly decrease as substrate stiffness decreases. Consequently, bonds are more likely to break on softer substrates, resulting in enhanced cell mobility.</p> </abstract>

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15

Venugopal, Balu, Pankaj Mogha, Jyotsna Dhawan, and Abhijit Majumder. "Cell density overrides the effect of substrate stiffness on human mesenchymal stem cells’ morphology and proliferation." Biomaterials Science 6, no. 5 (2018): 1109–19. http://dx.doi.org/10.1039/c7bm00853h.

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16

Simsek, Ahmet Nihat, Andrea Braeutigam, Matthias D. Koch, Joshua W. Shaevitz, Yunfei Huang, Gerhard Gompper, and Benedikt Sabass. "Substrate-rigidity dependent migration of an idealized twitching bacterium." Soft Matter 15, no. 30 (2019): 6224–36. http://dx.doi.org/10.1039/c9sm00541b.

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17

Guo, Wei-hui, Margo T. Frey, Nancy A. Burnham, and Yu-li Wang. "Substrate Rigidity Regulates the Formation and Maintenance of Tissues." Biophysical Journal 90, no. 6 (March 2006): 2213–20. http://dx.doi.org/10.1529/biophysj.105.070144.

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18

O’Connor, Roddy S., Xueli Hao, Keyue Shen, Keenan Bashour, Tatiana Akimova, Wayne W. Hancock, Lance C. Kam, and Michael C. Milone. "Substrate Rigidity Regulates Human T Cell Activation and Proliferation." Journal of Immunology 189, no. 3 (June 25, 2012): 1330–39. http://dx.doi.org/10.4049/jimmunol.1102757.

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19

Voloshin, Arkady. "Modeling Cell Movement on a Substrate with Variable Rigidity." International journal of Biomedical Engineering and Science 3, no. 1 (January 30, 2016): 19–36. http://dx.doi.org/10.5121/ijbes.2016.3102.

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20

Douezan, Stéphane, Julien Dumond, and Françoise Brochard-Wyart. "Wetting transitions of cellular aggregates induced by substrate rigidity." Soft Matter 8, no. 17 (2012): 4578. http://dx.doi.org/10.1039/c2sm07418d.

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21

Tee, Shang-You, Jianping Fu, Christopher S. Chen, and Paul A. Janmey. "Cell Shape and Substrate Rigidity Both Regulate Cell Stiffness." Biophysical Journal 100, no. 3 (February 2011): 303a. http://dx.doi.org/10.1016/j.bpj.2010.12.1856.

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22

Tee, Shang-You, Jianping Fu, Christopher S. Chen, and Paul A. Janmey. "Cell Shape and Substrate Rigidity Both Regulate Cell Stiffness." Biophysical Journal 100, no. 5 (March 2011): L25—L27. http://dx.doi.org/10.1016/j.bpj.2010.12.3744.

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23

Poddar, Souvik, Aerial M. Pratt, Paul B. Orndorff, Arjan van der Vaart, Wade D. Van Horn, and Marcia Levitus. "Uracil-DNA glycosylase efficiency is modulated by substrate rigidity." Biophysical Journal 122, no. 3 (February 2023): 149a. http://dx.doi.org/10.1016/j.bpj.2022.11.1004.

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24

Alegre-Cebollada, Jorge, Carla Huerta-Lopez, Alejandro Clemente-Manteca, Diana Velazquez-Carreras, Francisco M. Espinosa, Pablo Saez, Alvaro Martinez-del-Pozo, et al. "Cell response to substrate energy dissipation outweighs rigidity sensing." Biophysical Journal 122, no. 3 (February 2023): 292a. http://dx.doi.org/10.1016/j.bpj.2022.11.1652.

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25

Schmidt, Thomas, Hayri E. Balcioglu, Rolf Harkes, and Erik H. J. Danen. "Substrate Rigidity Modulates the Composition in Cell-Matrix Adhesions." Biophysical Journal 114, no. 3 (February 2018): 19a. http://dx.doi.org/10.1016/j.bpj.2017.11.149.

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26

Krivitskaya, Alexandra V., and Maria G. Khrenova. "Influence of the Active Site Flexibility on the Efficiency of Substrate Activation in the Active Sites of Bi-Zinc Metallo-β-Lactamases." Molecules 27, no. 20 (October 18, 2022): 7031. http://dx.doi.org/10.3390/molecules27207031.

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The influence of the active site flexibility on the efficiency of catalytic reaction is studied by taking two members of metallo-β-lactamases, L1 and NDM-1, with the same substrate, imipenem. Active sites of these proteins are covered by L10 loops, and differences in their amino acid compositions affect their rigidity. A more flexible loop in the NDM-1 brings additional flexibility to the active site in the ES complex. This is pronounced in wider distributions of key interatomic distances, such as the distance of the nucleophilic attack, coordination bond lengths, and covalent bond lengths in the substrate. Substrate activation, quantified by Fukui electrophilicity index of the carbonyl carbon atom of the substrate, is also sensitive to the active site flexibility. In the tighter and more rigid L1 enzyme-substrate complex, the substrate is activated more efficiently. In the NDM-1 containing system, only one third of the states are activated to the same extent. Other fractions demonstrate lower substrate activation. Efficiency of the substrate activation and rigidity of the ES complex influence the following chemical reaction. In the more rigid L1-containing system, the reaction barrier of the first step of the reaction is lower, and the first intermediate is more stabilized compared to the NDM-1 containing system.

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27

Lee, Jounghyun Helen, Neha Nataraj, Alex Dang, and Lance C. Kam. "Induction rate of regulatory T cells from conventional T cells is affected by substrate rigidity." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 176.20. http://dx.doi.org/10.4049/jimmunol.200.supp.176.20.

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Abstract The immune system maintains a balance between protection and tolerance. Regulatory T cells (Tregs) act as a tolerance mechanism to suppress effector immune cells. Recent studies suggest that the induction of Tregs from conventional T cells (Tconvs) has many practical and therapeutic advantages. Previously, both human and mouse T cells were reported to exhibit different responses to activating substrates of different rigidities as indicated in IL-2 secretion levels. In this work, we explore the previously unknown effect of substrate rigidity on the induction of Tregs from Tconvs. We used Sylgard 184 poly(dimethylsiloxane) (PDMS) to obtain rigidity ranging a few hundred kilopascals to megapascals. Mouse CD4+ T cells (Foxp3-GFP linked B6 mouse) were obtained from spleen and further isolated to CD25+ and CD25− cells using magnetic bead-based isolation kits. CD4+CD25− T cells (>99% Foxp3−) were then seeded onto the surfaces coated with antibodies to CD3 and CD28 in IL-2 and TGF-b-enriched media. Surprisingly, there was a significant increase in Treg induction rate at lower substrate rigidities (i.e., Young’s modulus, E ~ 100 kPa) compared to high rigidity (i.e., E ~ 3 MPa). To confirm that this significant difference in induction rate is truly related to T cell mechanosensing, we administered compound Y-27632 (cY) to inhibit myosin contractility. In the presence of cY, the difference in induction rate at varying rigidities was significantly reduced. This study furthers our understanding of mechanosensing properties of immune cells and raises questions about the underlying molecular mechanisms involved in this process of T cells choosing to proliferate or differentiate.

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28

Li, Shan, Li Juan Zheng, Cheng Yong Wang, Bing Miao Liao, and Lianyu Fu. "Micro drilling quality of the Cu/BT laminate for IC substrate." Circuit World 42, no. 2 (May 3, 2016): 55–62. http://dx.doi.org/10.1108/cw-03-2015-0006.

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Purpose In an integrated circuit (IC) substrate, more fillers, including talcum powder and aluminium hydroxide, are added, which leads to much higher rigidity and hardness compared with a traditional printed circuit board. However, the micro drilling of IC substrates is harder. This paper aims to test the drilling process of IC substrates to improve the drilling process and the micro hole quality. Design/methodology/approach Substrate drilling by a micro drill with 0.11-mm diameter was used under several drilling conditions. The influence of drilling conditions on the drilling process was observed. Drilling forces, drill wear and micro hole quality were also studied. Findings The deformation circle around holes, hole location accuracy, bugle hole and burrs were the major defects of micro holes that were observed during the drilling of the substrate. Reducing the drilling force and drill wear was the effective way to improve hole quality. Originality/value The technology and manufacturing of IC substrates has been little investigated. Research data on drilling IC substrates is lacking. The micro hole quality directly affects the reliability of IC substrates. Thus, improving the drilling technology of IC substrates is very important.

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29

Hsueh, Chun-Hway, and Pedro Miranda. "Modeling of contact-induced radial cracking in ceramic bilayer coatings on compliant substrates." Journal of Materials Research 18, no. 5 (May 2003): 1275–83. http://dx.doi.org/10.1557/jmr.2003.0175.

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Contact-induced radial cracking in ceramic coatings on compliant substrates was analyzed recently. Radial cracks initiate at the coating/substrate interface beneath the contact where maximum flexural tension occurs, and an analytical expression for the onset of radial cracking in monolayer coatings was formulated on the basis of the classical solution for flexing plates on elastic foundation. In the present study, the analytical expression was derived for the case of ceramic bilayer coatings on compliant substrates, which have significant applications in the structure of dental crowns. It was found that the analytical solution for bilayer-coating/substrate systems can be obtained from that of monolayer-coating/substrate systems by replacing the neutral surface position and the flexural rigidity of monolayer coating with those of bilayer coating. The predicted critical loads for initiating radial cracking were found to be in good agreement with existing measurements and finite element results for glass/alumina, glass/glass-ceramic, and glass/Y2O3-stabilized ZrO2polycrystal bilayers on polycarbonate substrates. Limitations of the present analysis are discussed.

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30

Lo, Chun-Min, Hong-Bei Wang, Micah Dembo, and Yu-li Wang. "Cell Movement Is Guided by the Rigidity of the Substrate." Biophysical Journal 79, no. 1 (July 2000): 144–52. http://dx.doi.org/10.1016/s0006-3495(00)76279-5.

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31

Ghassemi, S., G. Meacci, S. Liu, A. A. Gondarenko, A. Mathur, P. Roca-Cusachs, M. P. Sheetz, and J. Hone. "Cells test substrate rigidity by local contractions on submicrometer pillars." Proceedings of the National Academy of Sciences 109, no. 14 (March 19, 2012): 5328–33. http://dx.doi.org/10.1073/pnas.1119886109.

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32

Kostic, Ana, and Michael P. Sheetz. "Fibronectin Rigidity Response through Fyn and p130Cas Recruitment to the Leading Edge." Molecular Biology of the Cell 17, no. 6 (June 2006): 2684–95. http://dx.doi.org/10.1091/mbc.e05-12-1161.

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Cell motility on extracellular matrices critically depends on matrix rigidity, which affects cell adhesion and formation of focal contacts. Receptor-like protein tyrosine phosphatase alpha (RPTPα) and the αvβ3 integrin form a rigidity-responsive complex at the leading edge. Here we show that the rigidity response through increased spreading and growth correlates with leading edge recruitment of Fyn, but not endogenous c-Src. Recruitment of Fyn requires the palmitoylation site near the N-terminus and addition of that site to c-Src enables it to support a rigidity response. In all cases, the rigidity response correlates with the recruitment of the Src family kinase to early adhesions. The stretch-activated substrate of Fyn and c-Src, p130Cas, is also required for a rigidity response and it is phosphorylated at the leading edge in a Fyn-dependent process. A possible mechanism for the fibronectin rigidity response involves force-dependent Fyn phosphorylation of p130Cas with rigidity-dependent displacement. With the greater displacement of Fyn from p130Cas on softer surfaces, there will be less phosphorylation. These studies emphasize the importance of force and nanometer-level movements in cell growth and function.

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33

Podolnikova, Nataly P., Benjamin Bowen, Valeryi K. Lishko, Andriy V. Podolnikov, and Tatiana Ugarova. "Control of Platelet Adhesion by Rigidity Sensing at the Surface of Fibrin Clot." Blood 110, no. 11 (November 16, 2007): 3906. http://dx.doi.org/10.1182/blood.v110.11.3906.3906.

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Abstract Thrombus formation at sites of vascular injury must occur quickly to reduce blood loss, but is carefully controlled to limit vessel occlusion. Arrest of bleeding is mediated by adhesion and aggregation of platelets and the formation of the fibrin clot. While the interactions responsible for platelet adhesion and thrombus growth have been extensively researched, the mechanisms that limit platelet adhesion are not clear. We have previously demonstrated that plasma fibrinogen is a potent inhibitor of integrin-mediated leukocyte adhesion to fibrin clots and surface-bound fibrinogen, and have provided evidence that fibrinogen reduces cell adhesion by binding to the surface of fibrin rather than blocking leukocyte integrins. Accordingly, cells that engage fibrinogen molecules loosely bound to fibrin (soft substrate) are not able to consolidate their grip on the surface; subsequently, cells detach. Conversely, cells that adhere to the naked fibrin clot (rigid substrate) adhere firmly. Since fibrin and immobilized fibrinogen support platelet adhesion, we examined the effect of soluble fibrinogen on integrin αIIbβ3-mediated adhesion. We show that the anti-adhesive fibrinogen layer formed on the surface of fibrin inhibits platelet adhesion. We also demonstrate that fibrinogen immobilized on plastic at high densities (>20 μg/ml) supports weak platelet adhesion whereas at low concentrations (∼2 μg/ml) it is highly adhesive. An investigation of the mechanism underlying differential platelet adhesion indicates that platelet adhesion to rigid substrates (low-density fibrinogen and naked fibrin gel) induces much stronger phosphorylation of FAK and Syk kinases than that to soft substrates (high-density fibrinogen and fibrin exposed to soluble fibrinogen). Furthermore, the rigid, but not the soft substrates induce recruitment of signaling molecules talin and skelemin to αIIbβ3-containing focal adhesions. Consistent with their limited ability to induce sufficient signaling, soft substrates do not support platelet spreading. These data suggest that circulating fibrinogen prevents stable platelet adhesion by modifying the mechanical properties of the fibrin clot’s surface which results in reduced force generation and insufficient signaling.

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34

Shi, Lingting, and Lance Kam. "Substrate rigidity affects human regulatory T cell induction in vitro." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 230.11. http://dx.doi.org/10.4049/jimmunol.204.supp.230.11.

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Abstract Immunotherapy using regulatory T cells (Tregs) has shown recent successes in the treatment of autoimmune diseases. While natural Tregs are unstable and dysfunctional in the inflammatory milieu, induced Tregs are more potent and durable. Tregs can be induced from CD4+CD25− T cells in vitro with TGF-β and IL-2 during activation. Chemical pathways in Treg induction have been heavily investigated, but the impact of mechanical cues has not been thoroughly explored. As T cell activation has been shown to be sensitive to the substrate rigidity, Treg induction may also be mechanosensitive. To test this hypothesis, Tregs were induced on polyacrylamide gels of different rigidities (Young’s modulus of 5 to 110 kPa) coated with anti-CD3 and anti-CD28 for 72 hrs. The stiffer substrate significantly increased Treg induction, measured by percent FoxP3 high T cells. To further understand this process, single cell RNA-Seq analysis was performed on cells induced on 5 and 110 kPa gels, which revealed three clusters including conventional CD4+ cells, transition cells, and Tregs. For 5 kPa substrates, a higher proportion of cells expressed the FOXP3 genes than detected protein, whereas the proportions of cells that express the FOXP3 gene and protein were consistent on the 110 kPa gels. FOXP3+ cells on the softer gel also showed upregulation of genes that encode for ribosomal proteins and proteasomes. Thus, there could be some mechanism inhibiting expression or promoting degradation of FoxP3 protein in 5 kPa. Lastly, the induced Tregs in two groups exhibited different cell cycle profiles. These results indicated the mechanosensitive nature of Treg induction, which can assist in the biomaterial design for generating Tregs to advance Treg adoptive therapy.

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Hirata, Hiroaki, Keng-Hwee Chiam, Chwee Teck Lim, and Masahiro Sokabe. "Actin flow and talin dynamics govern rigidity sensing in actin–integrin linkage through talin extension." Journal of The Royal Society Interface 11, no. 99 (October 6, 2014): 20140734. http://dx.doi.org/10.1098/rsif.2014.0734.

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At cell–substrate adhesion sites, the linkage between actin filaments and integrin is regulated by mechanical stiffness of the substrate. Of potential molecular regulators, the linker proteins talin and vinculin are of particular interest because mechanical extension of talin induces vinculin binding with talin, which reinforces the actin–integrin linkage. For understanding the molecular and biophysical mechanism of rigidity sensing at cell–substrate adhesion sites, we constructed a simple physical model to examine a role of talin extension in the stiffness-dependent regulation of actin–integrin linkage. We show that talin molecules linking between retrograding actin filaments and substrate-bound integrin are extended in a manner dependent on substrate stiffness. The model predicts that, in adhesion complexes containing ≈30 talin links, talin is extended enough for vinculin binding when the substrate is stiffer than 1 kPa. The lifetime of talin links needs to be 2–5 s to achieve an appropriate response of talin extension against substrate stiffness. Furthermore, changes in actin velocity drastically shift the range of substrate stiffness that induces talin–vinculin binding. Our results suggest that talin extension is a key step in sensing and responding to substrate stiffness at cell adhesion sites.

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Mantena, P. Raju, Tezeswi Tadepalli, Brahmananda Pramanik, Veera M. Boddu, Matthew W. Brenner, L. David Stephenson, and Ashok Kumar. "Energy Dissipation and the High-Strain Rate Dynamic Response of Vertically Aligned Carbon Nanotube Ensembles Grown on Silicon Wafer Substrate." Journal of Nanomaterials 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/259458.

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The dynamic mechanical behavior and high-strain rate response characteristics of a functionally graded material (FGM) system consisting of vertically aligned carbon nanotube ensembles grown on silicon wafer substrate (VACNT-Si) are presented. Flexural rigidity (storage modulus) and loss factor (damping) were measured with a dynamic mechanical analyzer in an oscillatory three-point bending mode. It was found that the functionally graded VACNT-Si exhibited significantly higher damping without sacrificing flexural rigidity. A Split-Hopkinson pressure bar (SHPB) was used for determining the system response under high-strain rate compressive loading. Combination of a soft and flexible VACNT forest layer over the hard silicon substrate presented novel challenges for SHPB testing. It was observed that VACNT-Si specimens showed a large increase in the specific energy absorption over a pure Si wafer.

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GEORGES, PENELOPE C., ILYA LEVENTAL, WILFREDO De JESúS ROJAS, R. TYLER MILLER, and PAUL A. JANMEY. "EFFECT OF SUBSTRATE STIFFNESS ON THE STRUCTURE AND FUNCTION OF CELLS." Biophysical Reviews and Letters 01, no. 04 (October 2006): 401–10. http://dx.doi.org/10.1142/s1793048006000331.

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Most biological tissues are soft viscoelastic materials with elastic moduli ranging from approximately 100 to 100,000 Pa. Recent studies have examined the effect of substrate rigidity on cell structure and function, and many, but not all cell types exhibit a strong response to substrate stiffness. Some blood cells such as platelets and neutrophils have indistinguishable structures on hard and soft materials as long as they are sufficiently adhesive, whereas many cell types, including fibroblasts and endothelial cells spread much more strongly on rigid compared to soft substrates. A few cell types such as neurons appear to extend better on very soft materials. The different response of astrocytes and neurons to the stiffness of their substrate results in preferential growth of neurons on soft gels and astrocytes on hard gels, and suggests that preventing rigidification of damaged central nervous system tissue after injury may have utility in wound healing. How cells sense substrate stiffness is unknown. One candidate protein, filamin A, which responds to externally derived stresses, was tested in melanoma cells. Cells devoid of filamin A retain the ability to sense substrate stiffness, suggesting that other proteins are required for stiffness sensing.

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Balcioglu, Hayri E., Rolf Harkes, Erik H. J. Danen, and Thomas Schmidt. "Substrate rigidity modulates traction forces and stoichiometry of cell–matrix adhesions." Journal of Chemical Physics 156, no. 8 (February 28, 2022): 085101. http://dx.doi.org/10.1063/5.0077004.

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In cell–matrix adhesions, integrin receptors and associated proteins provide a dynamic coupling of the extracellular matrix (ECM) to the cytoskeleton. This allows bidirectional transmission of forces between the ECM and the cytoskeleton, which tunes intracellular signaling cascades that control survival, proliferation, differentiation, and motility. The quantitative relationships between recruitment of distinct cell–matrix adhesion proteins and local cellular traction forces are not known. Here, we applied quantitative super-resolution microscopy to cell–matrix adhesions formed on fibronectin-stamped elastomeric pillars and developed an approach to relate the number of talin, vinculin, paxillin, and focal adhesion kinase (FAK) molecules to the local cellular traction force. We find that FAK recruitment does not show an association with traction-force application, whereas a ∼60 pN force increase is associated with the recruitment of one talin, two vinculin, and two paxillin molecules on a substrate with an effective stiffness of 47 kPa. On a substrate with a fourfold lower effective stiffness, the stoichiometry of talin:vinculin:paxillin changes to 2:12:6 for the same ∼60 pN traction force. The relative change in force-related vinculin recruitment indicates a stiffness-dependent switch in vinculin function in cell–matrix adhesions. Our results reveal a substrate-stiffness-dependent modulation of the relationship between cellular traction-force and the molecular stoichiometry of cell–matrix adhesions.

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Sun, Yubing, Liang-Ting Jiang, Ryoji Okada, and Jianping Fu. "UV-Modulated Substrate Rigidity for Multiscale Study of Mechanoresponsive Cellular Behaviors." Langmuir 28, no. 29 (July 12, 2012): 10789–96. http://dx.doi.org/10.1021/la300978x.

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Frey, Margo T., and Yu-li Wang. "A photo-modulatable material for probing cellular responses to substrate rigidity." Soft Matter 5, no. 9 (2009): 1918. http://dx.doi.org/10.1039/b818104g.

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41

Watanabe, Takamitsu, Rebecca P. Lawson, Ylva S. E. Walldén, and Geraint Rees. "A Neuroanatomical Substrate Linking Perceptual Stability to Cognitive Rigidity in Autism." Journal of Neuroscience 39, no. 33 (June 18, 2019): 6540–54. http://dx.doi.org/10.1523/jneurosci.2831-18.2019.

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42

Wong, Stephanie, Wei-Hui Guo, and Yu-Li Wang. "Fibroblasts probe substrate rigidity with filopodia extensions before occupying an area." Proceedings of the National Academy of Sciences 111, no. 48 (November 17, 2014): 17176–81. http://dx.doi.org/10.1073/pnas.1412285111.

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43

Higgs, Henry N. "The harder the better: effects of substrate rigidity on cell motility." Trends in Biochemical Sciences 25, no. 9 (September 2000): 427. http://dx.doi.org/10.1016/s0968-0004(00)01653-4.

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44

Nemir, Stephanie, and Jennifer L. West. "Synthetic Materials in the Study of Cell Response to Substrate Rigidity." Annals of Biomedical Engineering 38, no. 1 (October 9, 2009): 2–20. http://dx.doi.org/10.1007/s10439-009-9811-1.

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45

Breuls, Roel, Astrid Bakker, Ruud Bank, Vincent Everts, and Theo Smit. "SUBSTRATE RIGIDITY AND EXTRACELLULAR MATRIX COMPOSITION INTERACT TO DETERMINE CELL BEHAVIOR." Journal of Biomechanics 41 (July 2008): S461. http://dx.doi.org/10.1016/s0021-9290(08)70460-3.

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Barreto, Sara, Cécile M. Perrault, and Damien Lacroix. "EFFECT OF THE CYTOSKELETON FIBERS AND SUBSTRATE RIGIDITY ON ADHERENT CELLS." Journal of Biomechanics 45 (July 2012): S418. http://dx.doi.org/10.1016/s0021-9290(12)70419-0.

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Sarkar, Anwesha, and Xuefeng Wang. "Integrin Molecular Tensions in Live Cells are Altered by Substrate Rigidity." Biophysical Journal 114, no. 3 (February 2018): 324a. http://dx.doi.org/10.1016/j.bpj.2017.11.1818.

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48

Kim, Tae-Jin, Jihye Seong, Mingxing Ouyang, Jie Sun, Shaoying Lu, Jun Pyu Hong, Ning Wang, and Yingxiao Wang. "Substrate rigidity regulates Ca2+oscillation via RhoA pathway in stem cells." Journal of Cellular Physiology 218, no. 2 (February 2009): 285–93. http://dx.doi.org/10.1002/jcp.21598.

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49

Zheng, Yonggang, Huayuan Tang, Hongfei Ye, and Hongwu Zhang. "Adhesion and bending rigidity-mediated wrapping of carbon nanotubes by a substrate-supported cell membrane." RSC Advances 5, no. 54 (2015): 43772–79. http://dx.doi.org/10.1039/c5ra04426j.

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The adhesion and bending rigidity-mediated wrapping of carbon nanotubes by a substrate-supported cell membrane has been explored and phase diagrams that characterize the effect of the energy competition on the equilibrium configuration have been presented.

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50

Suhir, E. "How Compliant Should a Die-Attachment be to Protect the Chip From Substrate Bowing?" Journal of Electronic Packaging 117, no. 1 (March 1, 1995): 88–92. http://dx.doi.org/10.1115/1.2792073.

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The purpose of the analysis is to find out whether die attachment can be made compliant enough to protect the chip from excessive bowing of the substrate. We showed that in a typical situation, when the substrate (card) has a significantly larger flexural rigidity than the chip, the mechanical behavior of the chip-substrate assembly is governed by a parameter u=lK/4D14, where l is half the chip’s length, D1 is its flexural rigidity, and K is the through thickness spring constant of the attachment. We found that in order for a die attachment to have an appreciable effect on chip bowing, this parameter should be considerably smaller than 2.5. In the performed numerical example, for a 2 rail thick die attachment, this value corresponds to Young’s modulus of only 2300 psi. Therefore we conclude that conventional epoxy adhesives cannot provide sufficient buffering effect in this case, and, if such adhesives are used, the curvature of the die will be practically the same as the curvature of the substrate. In this situation, thinner dies will result in lower bending stresses. However, if low modulus die attachment materials, such as silicone gels, are considered, then employment of thicker dies might be advisable.

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