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1

Swiatlowska, Pamela, Jose L. Sanchez-Alonso, Peter T. Wright, Pavel Novak, and Julia Gorelik. "Microtubules regulate cardiomyocyte transversal Young’s modulus." Proceedings of the National Academy of Sciences 117, no. 6 (January 27, 2020): 2764–66. http://dx.doi.org/10.1073/pnas.1917171117.

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The field of cardiomyocyte mechanobiology is gaining significant attention, due to accumulating evidence concerning the significant role of cellular mechanical effects on the integrated function of the heart. To date, the protein titin has been demonstrated as a major contributor to the cardiomyocytes Young’s modulus (YM). The microtubular network represents another potential regulator of cardiac mechanics. However, the contribution of microtubules (MTs) to the membrane YM is still understudied and has not been interrogated in the context of myocardial infarction (MI) or mechanical loading and unloading. Using nanoscale mechanoscanning ion conductance microscopy, we demonstrate that MTs contribute to cardiomyocyte transverse YM in healthy and pathological states with different mechanical loading. Specifically, we show that posttranslational modifications of MTs have differing effects on cardiomyocyte YM: Acetylation provides flexibility, whereas detyrosination imparts rigidity. Further studies demonstrate that there is no correlation between the total protein amount of acetylated and detyrosinated MT. Yet, in the polymerized-only populations, an increased level of acetylation results in a decline of detyrosinated MTs in an MI model.
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2

Pan, Xuan Sabrina, Jiewen Li, Edward B. Brown, and Catherine K. Kuo. "Embryo movements regulate tendon mechanical property development." Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1759 (September 24, 2018): 20170325. http://dx.doi.org/10.1098/rstb.2017.0325.

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Tendons transmit forces from muscles to bones to enable skeletal motility. During development, tendons begin to bear load at the onset of embryo movements. Using the chick embryo model, this study showed that altered embryo movement frequency led to changes in elastic modulus of calcaneal tendon. In particular, paralysis led to decreased modulus, whereas hypermotility led to increased modulus. Paralysis also led to reductions in activity levels of lysyl oxidase (LOX), an enzyme that we previously showed is required for cross-linking-mediated elaboration of tendon mechanical properties. Additionally, inhibition of LOX activity abrogated hypermotility-induced increases in modulus. Taken together, our findings suggest embryo movements are critical for tendon mechanical property development and implicate LOX in this process. These exciting findings expand current knowledge of how functional tendons form during development and could guide future clinical approaches to treat tendon defects associated with abnormal mechanical loading in utero . This article is part of the Theo Murphy meeting issue ‘Mechanics of development’.
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Ebner, Michael, and Volker Haucke. "Mechanical signals regulate TORC2 activity." Nature Cell Biology 20, no. 9 (August 28, 2018): 994–95. http://dx.doi.org/10.1038/s41556-018-0181-5.

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Cui, Xin, Jie Tong, Jimmy Yau, Apratim Bajpai, Jing Yang, Yansong Peng, Mrinalini Singh, Weiyi Qian, Xiao Ma, and Weiqiang Chen. "Mechanical Forces Regulate Asymmetric Vascular Cell Alignment." Biophysical Journal 119, no. 9 (November 2020): 1771–80. http://dx.doi.org/10.1016/j.bpj.2020.09.020.

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5

Stamenović, Dimitrije, and Ning Wang. "Invited Review: Engineering approaches to cytoskeletal mechanics." Journal of Applied Physiology 89, no. 5 (November 1, 2000): 2085–90. http://dx.doi.org/10.1152/jappl.2000.89.5.2085.

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An outstanding problem in cell biology is how cells sense mechanical forces and how those forces affect cellular functions. Various biophysical and biochemical mechanisms have been invoked to answer this question. A growing body of evidence indicates that the deformable cytoskeleton (CSK), an intracellular network of interconnected filamentous biopolymers, provides a physical basis for transducing mechanical signals into biochemical signals. Therefore, to understand how mechanical forces regulate cellular functions, it is important to know how cells respond to changes in the CSK force balance and to identify the underlying mechanisms that control transmission of mechanical forces throughout the CSK and bring it to equilibrium. Recent developments of new experimental techniques for measuring cell mechanical properties and novel theoretical models of cellular mechanics make it now possible to identify and quantitate the contributions of various CSK structures to the overall balance of mechanical forces in the cell. This review focuses on engineering approaches that have been used in the past two decades in studies of the mechanics of the CSK.
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6

Ruehle, M. A., E. A. Eastburn, S. A. LaBelle, L. Krishnan, J. A. Weiss, J. D. Boerckel, L. B. Wood, R. E. Guldberg, and N. J. Willett. "Extracellular matrix compression temporally regulates microvascular angiogenesis." Science Advances 6, no. 34 (August 2020): eabb6351. http://dx.doi.org/10.1126/sciadv.abb6351.

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Mechanical cues influence tissue regeneration, and although vasculature is known to be mechanically sensitive, little is known about the effects of bulk extracellular matrix deformation on the nascent vessel networks found in healing tissues. Previously, we found that dynamic matrix compression in vivo potently regulated revascularization during bone tissue regeneration; however, whether matrix deformations directly regulate angiogenesis remained unknown. Here, we demonstrated that load initiation time, magnitude, and mode all regulate microvascular growth, as well as upstream angiogenic and mechanotransduction signaling pathways. Immediate load initiation inhibited angiogenesis and expression of early sprout tip cell selection genes, while delayed loading enhanced microvascular network formation and upstream signaling pathways. This research provides foundational understanding of how extracellular matrix mechanics regulate angiogenesis and has critical implications for clinical translation of new regenerative medicine therapies and physical rehabilitation strategies designed to enhance revascularization during tissue regeneration.
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7

Eckes, Beate, Manon C. Zweers, Zhi Gang Zhang, Ralf Hallinger, Cornelia Mauch, Monique Aumailley, and Thomas Krieg. "Mechanical Tension and Integrin α2β1 Regulate Fibroblast Functions." Journal of Investigative Dermatology Symposium Proceedings 11, no. 1 (September 2006): 66–72. http://dx.doi.org/10.1038/sj.jidsymp.5650003.

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8

Veeriah, Vimal, Riccardo Paone, Suvro Chatterjee, Anna Teti, and Mattia Capulli. "Osteoblasts Regulate Angiogenesis in Response to Mechanical Unloading." Calcified Tissue International 104, no. 3 (November 21, 2018): 344–54. http://dx.doi.org/10.1007/s00223-018-0496-z.

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9

Barnes, J. Matthew, Laralynne Przybyla, and Valerie M. Weaver. "Tissue mechanics regulate brain development, homeostasis and disease." Journal of Cell Science 130, no. 1 (January 1, 2017): 71–82. http://dx.doi.org/10.1242/jcs.191742.

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10

Chocholoušek, M., Z. Fulín, and J. Janoušek. "Vývoj autoklávu pro zkoušení materiálù v prostøedí tìžkých tekutých kovù / Development of autoclave for testing materials in the environment of heavy liquid metals." Koroze a ochrana materialu 59, no. 3 (November 1, 2015): 73–76. http://dx.doi.org/10.1515/kom-2015-0017.

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V rámci projektu SUSEN rozšiřuje společnost CVŘ oblast výzkumu na prostředí těžkých tekutých kovů se zaměřením korozního vlivu média na mechanické vlastnosti materiálů. Součástí je vývoj korozních autoklávů pro zkoušení tahových a únavových vlastností a také vlastností v oblasti tečení. Zkušební cela je určena pro zkoušky do teplot 600 °C s regulací obsahu kyslíku v médiu (olovo, eutektikum olovo-bismut). Pro zabezpečení těsnosti a umožnění regulace obsahu kyslíku je v systému udržována ochranná atmosféra argonu s provozním přetlakem do 2 bar. Systém je řešen jako dvoukomorové provedení, kde jedna komora slouží k přípravě korozního média a druhá komora je určena pro materiálové zkoušky. Tavící komora je řešena jako mobilní cela, kterou je možno připojit na další zkušební cely a provést přečerpání média. Zkušební cely jsou umístěny v pracovním prostoru zkušebních strojů a dimenzovány na maximální tahové zatížení 10 kN. Jsou vybaveny adaptéry pro uchycení tyčových vzorků bez závitových hlav a malých CT-vzorků. Navazující činnost bude zaměřena na vývoj měření deformace v tekutých těžkých kovech.
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11

Chan, C. J., G. Whyte, L. Boyde, G. Salbreux, and J. Guck. "Impact of heating on passive and active biomechanics of suspended cells." Interface Focus 4, no. 2 (April 6, 2014): 20130069. http://dx.doi.org/10.1098/rsfs.2013.0069.

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A cell is a complex material whose mechanical properties are essential for its normal functions. Heating can have a dramatic effect on these mechanical properties, similar to its impact on the dynamics of artificial polymer networks. We investigated such mechanical changes by the use of a microfluidic optical stretcher, which allowed us to probe cell mechanics when the cells were subjected to different heating conditions at different time scales. We find that HL60/S4 myeloid precursor cells become mechanically more compliant and fluid-like when subjected to either a sudden laser-induced temperature increase or prolonged exposure to higher ambient temperature. Above a critical temperature of 52 ± 1°C, we observed active cell contraction, which was strongly correlated with calcium influx through temperature-sensitive transient receptor potential vanilloid 2 (TRPV2) ion channels, followed by a subsequent expansion in cell volume. The change from passive to active cellular response can be effectively described by a mechanical model incorporating both active stress and viscoelastic components. Our work highlights the role of TRPV2 in regulating the thermomechanical response of cells. It also offers insights into how cortical tension and osmotic pressure govern cell mechanics and regulate cell-shape changes in response to heat and mechanical stress.
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12

Rowley, J. A., Z. Sun, D. Goldman, and D. J. Mooney. "Biomaterials to Spatially Regulate Cell Fate." Advanced Materials 14, no. 12 (June 18, 2002): 886. http://dx.doi.org/10.1002/1521-4095(20020618)14:12<886::aid-adma886>3.0.co;2-i.

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13

Ajeti, Visar, A. Pasha Tabatabai, Andrew J. Fleszar, Michael F. Staddon, Daniel S. Seara, Cristian Suarez, M. Sulaiman Yousafzai, et al. "Wound healing coordinates actin architectures to regulate mechanical work." Nature Physics 15, no. 7 (April 8, 2019): 696–705. http://dx.doi.org/10.1038/s41567-019-0485-9.

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14

Lichter, Jenny A., M. Todd Thompson, Maricela Delgadillo, Takehiro Nishikawa, Michael F. Rubner, and Krystyn J. Van Vliet. "Substrata Mechanical Stiffness Can Regulate Adhesion of Viable Bacteria." Biomacromolecules 9, no. 6 (June 2008): 1571–78. http://dx.doi.org/10.1021/bm701430y.

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15

Lichter, Jenny A., M. Todd Thompson, Maricela Delgadillo, Takehiro Nishikawa, Michael F. Rubner, and Krystyn J. Van Vliet. "Substrata Mechanical Stiffness Can Regulate Adhesion of Viable Bacteria." Biomacromolecules 9, no. 10 (October 13, 2008): 2967. http://dx.doi.org/10.1021/bm8009335.

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16

Saldaña, Laura, Lara Crespo, Fátima Bensiamar, Manuel Arruebo, and Nuria Vilaboa. "Mechanical forces regulate stem cell response to surface topography." Journal of Biomedical Materials Research Part A 102, no. 1 (April 24, 2013): 128–40. http://dx.doi.org/10.1002/jbm.a.34674.

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17

Calve, Sarah, and Hans‐Georg Simon. "Biochemical and mechanical environment cooperatively regulate skeletal muscle regeneration." FASEB Journal 26, no. 6 (March 13, 2012): 2538–45. http://dx.doi.org/10.1096/fj.11-200162.

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18

Lü, Tie-Yu, Hai Feng, Yufeng Zhang, Yuerui Lu, and Jin-Cheng Zheng. "Regulate the polarity of phosphorene’s mechanical properties by oxidation." Computational Materials Science 139 (November 2017): 341–46. http://dx.doi.org/10.1016/j.commatsci.2017.08.021.

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19

Souza, Daniel, Marcelo Lemos Rossi, Flávio Keocheguerians, Vinícius Castanheira do Nascimento, Louriel Oliveira Vilarinho, and Américo Scotti. "Influência da regulagem de parâmetros de soldagem sobre a estabilidade do processo MIG/MAG operando em curto-circuito." Soldagem & Inspeção 16, no. 1 (March 2011): 22–32. http://dx.doi.org/10.1590/s0104-92242011000100004.

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Devido ao potencial de aplicabilidade do processo MIG/MAG no modo de transferência por curto-circuito, torna-se importante o pleno entendimento da regulagem dos parâmetros sobre a estabilidade da transferência metálica e suas conseqüências sobre a geração de respingos. Soldagens de simples deposição sobre chapas foram realizadas para verificar a influência da variação da tensão, DBCP e das taxas de crescimento e decrescimento da corrente na estabilidade da transferência por curto-circuito, utilizando-se como gás de proteção 3 misturas largamente utilizadas na prática. Como critério de comparação, foi quantificada a regularidade da transferência através de um índice a partir do comportamento do sinal de tensão de soldagem. Os resultados mostram que, operando em curtocircuito, a tensão regulada tem forte influência sobre a estabilidade de transferência, existindo uma faixa ótima. Esta faixa é fortemente influenciada pelo tipo de gás, valor da corrente, DBCP e regulagem do fator de indução. Quanto menor o teor de CO2, mais regular se torna a transferência. O efeito do fator indutivo depende do teor de CO2 na mistura.
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20

Rydholm, Susanna, Gordon Zwartz, Jacob M. Kowalewski, Padideh Kamali-Zare, Thomas Frisk, and Hjalmar Brismar. "Mechanical properties of primary cilia regulate the response to fluid flow." American Journal of Physiology-Renal Physiology 298, no. 5 (May 2010): F1096—F1102. http://dx.doi.org/10.1152/ajprenal.00657.2009.

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The primary cilium is a ubiquitous organelle present on most mammalian cells. Malfunction of the organelle has been associated with various pathological disorders, many of which lead to cystic disorders in liver, pancreas, and kidney. Primary cilia have in kidney epithelial cells been observed to generate intracellular calcium in response to fluid flow, and disruption of proteins involved in this calcium signaling lead to autosomal dominant polycystic kidney disease, implying a direct connection between calcium signaling and cyst formation. It has also been shown that there is a significant lag between the onset of flow and initiation of the calcium signal. The present study focuses on the mechanics of cilium bending and the resulting calcium signal. Visualization of real-time cilium movements in response to different types of applied flow showed that the bending is fast compared with the initiation of calcium increase. Mathematical modeling of cilium and surrounding membrane was performed to deduce the relation between bending and membrane stress. The results showed a delay in stress buildup that was similar to the delay in calcium signal. Our results thus indicate that the delay in calcium response upon cilia bending is caused by mechanical properties of the cell membrane.
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Yang, Chun, Frank W. DelRio, Hao Ma, Anouk R. Killaars, Lena P. Basta, Kyle A. Kyburz, and Kristi S. Anseth. "Spatially patterned matrix elasticity directs stem cell fate." Proceedings of the National Academy of Sciences 113, no. 31 (July 19, 2016): E4439—E4445. http://dx.doi.org/10.1073/pnas.1609731113.

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There is a growing appreciation for the functional role of matrix mechanics in regulating stem cell self-renewal and differentiation processes. However, it is largely unknown how subcellular, spatial mechanical variations in the local extracellular environment mediate intracellular signal transduction and direct cell fate. Here, the effect of spatial distribution, magnitude, and organization of subcellular matrix mechanical properties on human mesenchymal stem cell (hMSCs) function was investigated. Exploiting a photodegradation reaction, a hydrogel cell culture substrate was fabricated with regions of spatially varied and distinct mechanical properties, which were subsequently mapped and quantified by atomic force microscopy (AFM). The variations in the underlying matrix mechanics were found to regulate cellular adhesion and transcriptional events. Highly spread, elongated morphologies and higher Yes-associated protein (YAP) activation were observed in hMSCs seeded on hydrogels with higher concentrations of stiff regions in a dose-dependent manner. However, when the spatial organization of the mechanically stiff regions was altered from a regular to randomized pattern, lower levels of YAP activation with smaller and more rounded cell morphologies were induced in hMSCs. We infer from these results that irregular, disorganized variations in matrix mechanics, compared with regular patterns, appear to disrupt actin organization, and lead to different cell fates; this was verified by observations of lower alkaline phosphatase (ALP) activity and higher expression of CD105, a stem cell marker, in hMSCs in random versus regular patterns of mechanical properties. Collectively, this material platform has allowed innovative experiments to elucidate a novel spatial mechanical dosing mechanism that correlates to both the magnitude and organization of spatial stiffness.
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Lenzini, Stephen, Raymond Bargi, Gina Chung, and Jae-Won Shin. "Matrix mechanics and water permeation regulate extracellular vesicle transport." Nature Nanotechnology 15, no. 3 (February 17, 2020): 217–23. http://dx.doi.org/10.1038/s41565-020-0636-2.

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23

Kirkland, Natalie J., Alice C. Yuen, Melda Tozluoglu, Nancy Hui, Ewa K. Paluch, and Yanlan Mao. "Tissue Mechanics Regulate Mitotic Nuclear Dynamics during Epithelial Development." Current Biology 30, no. 13 (July 2020): 2419–32. http://dx.doi.org/10.1016/j.cub.2020.04.041.

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24

Warner, Mark. "Topographic Mechanics and Applications of Liquid Crystalline Solids." Annual Review of Condensed Matter Physics 11, no. 1 (March 10, 2020): 125–45. http://dx.doi.org/10.1146/annurev-conmatphys-031119-050738.

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Liquid crystal elastomers and glasses suffer huge length changes on heating, illumination, exposure to humidity, etc. A challenge is to program these changes to give a complex mechanical response for micromachines and soft robotics. Also desirable can be strong response, where bend is avoided in favor of stretch and compression, even in the slender shells that are our subject. A new mechanics paradigm arises from such materials—spatially programmed anisotropy allows a spatially varying metric to develop upon stimulation, with evolving Gaussian curvature, topography changes, and superstrong actuation. We call this metric mechanics or topographical mechanics. Thus programmed, liquid crystalline solids meet the above aims. A frontier is the complete programming and control of topography, driving both Gaussian and mean curvature evolution. That, and smart shells, which sense and self-regulate, and exotic new realizations of anisotropic responsive structures, are our concluding themes.
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Wu, Qingqing, Yue Li, Mohan Lyu, Yiwen Luo, Hui Shi, and Shangwei Zhong. "Touch-induced seedling morphological changes are determined by ethylene-regulated pectin degradation." Science Advances 6, no. 48 (November 2020): eabc9294. http://dx.doi.org/10.1126/sciadv.abc9294.

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How mechanical forces regulate plant growth is a fascinating and long-standing question. After germination underground, buried seedlings have to dynamically adjust their growth to respond to mechanical stimulation from soil barriers. Here, we designed a lid touch assay and used atomic force microscopy to investigate the mechanical responses of seedlings during soil emergence. Touching seedlings induced increases in cell wall stiffness and decreases in cell elongation, which were correlated with pectin degradation. We revealed that PGX3, which encodes a polygalacturonase, mediates touch-imposed alterations in the pectin matrix and the mechanics of morphogenesis. Furthermore, we found that ethylene signaling is activated by touch, and the transcription factor EIN3 directly associates with PGX3 promoter and is required for touch-repressed PGX3 expression. By uncovering the link between mechanical forces and cell wall remodeling established via the EIN3-PGX3 module, this work represents a key step in understanding the molecular framework of touch-induced morphological changes.
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Chen, Xiaodong, Chundong Xue, and Guoqing Hu. "Confinements regulate capillary instabilities of fluid threads." Journal of Fluid Mechanics 873 (June 28, 2019): 816–34. http://dx.doi.org/10.1017/jfm.2019.426.

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We study the breakup of confined fluid threads at low flow rates to understand instability mechanisms. To determine the critical conditions between the earlier quasi-stable necking stage and the later unstable collapse stage, simulations and experiments are designed to operate at an extremely low flow rate. The critical mean radii at the neck centres are identified by the stop-flow method for elementary microfluidic configurations. Two distinct origins of capillary instabilities are revealed for different confinement situations. One is the gradient of capillary pressure induced by the confinements of geometry and external flow, whereas the other is the competition between the capillary pressure and internal pressure determined by the confinements.
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Ma, Fei‐He, Chang Li, Yang Liu, and Linqi Shi. "Mimicking Molecular Chaperones to Regulate Protein Folding." Advanced Materials 32, no. 3 (May 2, 2019): 1805945. http://dx.doi.org/10.1002/adma.201805945.

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28

dos Santos, Ália, and Christopher P. Toseland. "Regulation of Nuclear Mechanics and the Impact on DNA Damage." International Journal of Molecular Sciences 22, no. 6 (March 20, 2021): 3178. http://dx.doi.org/10.3390/ijms22063178.

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In eukaryotic cells, the nucleus houses the genomic material of the cell. The physical properties of the nucleus and its ability to sense external mechanical cues are tightly linked to the regulation of cellular events, such as gene expression. Nuclear mechanics and morphology are altered in many diseases such as cancer and premature ageing syndromes. Therefore, it is important to understand how different components contribute to nuclear processes, organisation and mechanics, and how they are misregulated in disease. Although, over the years, studies have focused on the nuclear lamina—a mesh of intermediate filament proteins residing between the chromatin and the nuclear membrane—there is growing evidence that chromatin structure and factors that regulate chromatin organisation are essential contributors to the physical properties of the nucleus. Here, we review the main structural components that contribute to the mechanical properties of the nucleus, with particular emphasis on chromatin structure. We also provide an example of how nuclear stiffness can both impact and be affected by cellular processes such as DNA damage and repair.
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Humphrey, Jay D., and Martin A. Schwartz. "Vascular Mechanobiology: Homeostasis, Adaptation, and Disease." Annual Review of Biomedical Engineering 23, no. 1 (July 13, 2021): 1–27. http://dx.doi.org/10.1146/annurev-bioeng-092419-060810.

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Cells of the vascular wall are exquisitely sensitive to changes in their mechanical environment. In healthy vessels, mechanical forces regulate signaling and gene expression to direct the remodeling needed for the vessel wall to maintain optimal function. Major diseases of arteries involve maladaptive remodeling with compromised or lost homeostatic mechanisms. Whereas homeostasis invokes negative feedback loops at multiple scales to mediate mechanobiological stability, disease progression often occurs via positive feedback that generates mechanobiological instabilities. In this review, we focus on the cell biology, wall mechanics, and regulatory pathways associated with arterial health and how changes in these processes lead to disease. We discuss how positive feedback loops arise via biomechanical and biochemical means. We conclude that inflammation plays a central role in overriding homeostatic pathways and suggest future directions for addressing therapeutic needs.
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Nee, Cheng Chu, Chia Pao Chang, and Tung Tsuan Tsay. "Temperature and Mechanical Stimuli to Regulate Pear and Papaya Growth." Engei Gakkai zasshi 67, no. 6 (1998): 1124–27. http://dx.doi.org/10.2503/jjshs.67.1124.

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31

Kasper, Grit, Niels Dankert, Jens Tuischer, Moritz Hoeft, Timo Gaber, Juliane D. Glaeser, Desiree Zander, et al. "Mesenchymal Stem Cells Regulate Angiogenesis According to Their Mechanical Environment." Stem Cells 25, no. 4 (April 2007): 903–10. http://dx.doi.org/10.1634/stemcells.2006-0432.

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32

Fox, A. M., J. Piascik, J. Y. Thompson, B. Koller, and A. J. Banes. "Nucleotides and nucleosides regulate mechanical integrity of mouse tail tendons." Journal of Biomechanics 39 (January 2006): S59. http://dx.doi.org/10.1016/s0021-9290(06)83117-9.

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Robbins, James R., Stephen P. Evanko, and Kathryn G. Vogel. "Mechanical Loading and TGF-β Regulate Proteoglycan Synthesis in Tendon." Archives of Biochemistry and Biophysics 342, no. 2 (June 1997): 203–11. http://dx.doi.org/10.1006/abbi.1997.0102.

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34

Canty, John. "Cargo Adaptors Regulate the Mechanical Properties of Mammalian Dynein-Dynactin." Biophysical Journal 116, no. 3 (February 2019): 409a. http://dx.doi.org/10.1016/j.bpj.2018.11.2206.

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35

Doyoung, K., and Y. Son. "Mechanical Cyclic Stretch Regulate Angiogenic Abilities of Endothelial Progenitor cells." Cytotherapy 22, no. 5 (May 2020): S191—S192. http://dx.doi.org/10.1016/j.jcyt.2020.04.051.

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36

Elshenawy, Mohamed, and Ahmet Yildiz. "Cargo Adaptors Regulate the Mechanical Properties of Dynein/Dynactin Complex." Biophysical Journal 114, no. 3 (February 2018): 512a. http://dx.doi.org/10.1016/j.bpj.2017.11.2798.

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37

Caggiano, Laura R., Jia-Jye Lee, and Jeffrey W. Holmes. "Surgical reinforcement alters collagen alignment and turnover in healing myocardial infarcts." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 4 (October 1, 2018): H1041—H1050. http://dx.doi.org/10.1152/ajpheart.00088.2018.

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Previous studies have suggested that the composition and global mechanical properties of the scar tissue that forms after a myocardial infarction (MI) are key determinants of long-term survival, and emerging therapies such as biomaterial injection are designed in part to alter those mechanical properties. However, recent evidence suggests that local mechanics regulate scar formation post-MI, so that perturbing infarct mechanics could have unexpected consequences. We therefore tested the effect of changes in local mechanical environment on scar collagen turnover, accumulation, and alignment in 77 Sprague-Dawley rats at 1, 2, 3 and 6 wk post-MI by sewing a Dacron patch to the epicardium to eliminate circumferential strain while permitting continued longitudinal stretching with each heart beat. We found that collagen in healing infarcts aligned parallel to regional strain and perpendicular to the preinfarction muscle and collagen fiber direction, strongly supporting our hypothesis that mechanical environment is the primary determinant of scar collagen alignment. Mechanical reinforcement reduced levels of carboxy-terminal propeptide of type I procollagen (PICP; a biomarker for collagen synthesis) in samples collected by microdialysis significantly, particularly in the first 2 wk. Reinforcement also reduced carboxy-terminal telopeptide of type I collagen (ICTP; a biomarker for collagen degradation), particularly at later time points. These alterations in collagen turnover produced no change in collagen area fraction as measured by histology but significantly reduced wall thickness in the reinforced scars compared with untreated controls. Our findings confirm the importance of regional mechanics in regulating scar formation after infarction and highlight the potential for therapies that reduce stretch to also reduce wall thickness in healing infarcts. NEW & NOTEWORTHY This study shows that therapies such as surgical reinforcement, which reduce stretch in healing infarcts, can also reduce collagen synthesis and wall thickness and modify collagen alignment in postinfarction scars.
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38

Chen, Xiaodong, Chundong Xue, and Guoqing Hu. "Confinements regulate capillary instabilities of fluid threads – CORRIGENDUM." Journal of Fluid Mechanics 873 (July 8, 2019): 1207. http://dx.doi.org/10.1017/jfm.2019.536.

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39

Muhamed, Ismaeel, Jun Wu, Poonam Sehgal, Xinyu Kong, Arash Tajik, Ning Wang, and Deborah E. Leckband. "E-cadherin-mediated force transduction signals regulate global cell mechanics." Journal of Cell Science 129, no. 9 (March 10, 2016): 1843–54. http://dx.doi.org/10.1242/jcs.185447.

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40

Weirich, Kimberly L., Samantha Stam, Edwin Munro, and Margaret L. Gardel. "Actin bundle architecture and mechanics regulate myosin II force generation." Biophysical Journal 120, no. 10 (May 2021): 1957–70. http://dx.doi.org/10.1016/j.bpj.2021.03.026.

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41

Taylor, A. F., M. M. Saunders, D. L. Shingle, J. M. Cimbala, Z. Zhou, and H. J. Donahue. "Mechanically stimulated osteocytes regulate osteoblastic activity via gap junctions." American Journal of Physiology-Cell Physiology 292, no. 1 (January 2007): C545—C552. http://dx.doi.org/10.1152/ajpcell.00611.2005.

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The strong correlation between a bone's architectural properties and the mechanical forces that it experiences has long been attributed to the existence of a cell that not only detects mechanical load but also structurally adapts the bone matrix to counter it. One of the most likely cellular candidates for such a “mechanostat” is the osteocyte, which resides within the mineralized bone matrix and is perfectly situated to detect mechanically induced signals. However, as osteocytes can neither form nor resorb bone, it has been hypothesized that they orchestrate mechanically induced bone remodeling by coordinating the actions of cells residing on the bone surface, such as osteoblasts. To investigate this hypothesis, we developed a novel osteocyte-osteoblast coculture model that mimics in vivo systems by permitting us to expose osteocytes to physiological levels of fluid shear while shielding osteoblasts from it. Our results show that osteocytes exposed to a fluid shear rate of 4.4 dyn/cm2 rapidly increase the alkaline phosphatase activity of the shielded osteoblasts and that osteocytic-osteoblastic physical contact is a prerequisite. Furthermore, both functional gap junctional intercellular communication and the mitogen-activated protein kinase, extracellular signal-regulated kinase 1/2 signaling pathway are essential components in the osteoblastic response to osteocyte communicated mechanical signals. By utilizing other nonosteocytic coculture models, we also show that the ability to mediate osteoblastic alkaline phosphatase levels in response to the application of fluid shear is a phenomena unique to osteocytes and is not reproduced by other mesenchymal cell types.
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42

Gardinier, Joseph, Weidong Yang, Gregory R. Madden, Andris Kronbergs, Vimal Gangadharan, Elizabeth Adams, Kirk Czymmek, and Randall L. Duncan. "P2Y2 receptors regulate osteoblast mechanosensitivity during fluid flow." American Journal of Physiology-Cell Physiology 306, no. 11 (June 1, 2014): C1058—C1067. http://dx.doi.org/10.1152/ajpcell.00254.2013.

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Mechanical stimulation of osteoblasts activates many cellular mechanisms including the release of ATP. Binding of ATP to purinergic receptors is key to load-induced osteogenesis. Osteoblasts also respond to fluid shear stress (FSS) with increased actin stress fiber formation (ASFF) that we postulate is in response to activation of the P2Y2 receptor (P2Y2R). Furthermore, we predict that ASFF increases cell stiffness and reduces the sensitivity to further mechanical stimulation. We found that small interfering RNA (siRNA) suppression of P2Y2R attenuated ASFF in response to FSS and ATP treatment. In addition, RhoA GTPase was activated within 15 min after the onset of FSS or ATP treatment and mediated ASFF following P2Y2R activation via the Rho kinase (ROCK)1/LIM kinase 2/cofilin pathway. We also observed that ASFF in response to FSS or ATP treatment increased the cell stiffness and was prevented by knocking down P2Y2R. Finally, we confirmed that the enhanced cell stiffness and ASFF in response to RhoA GTPase activation during FSS drastically reduced the mechanosensitivity of the osteoblasts based on the intracellular Ca2+ concentration ([Ca2+]i) response to consecutive bouts of FSS. These data suggest that osteoblasts can regulate their mechanosensitivity to continued load through P2Y2R activation of the RhoA GTPase signaling cascade, leading to ASFF and increased cell stiffness.
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43

Sun, Zhiqi, Shengzhen S. Guo, and Reinhard Fässler. "Integrin-mediated mechanotransduction." Journal of Cell Biology 215, no. 4 (November 8, 2016): 445–56. http://dx.doi.org/10.1083/jcb.201609037.

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Cells can detect and react to the biophysical properties of the extracellular environment through integrin-based adhesion sites and adapt to the extracellular milieu in a process called mechanotransduction. At these adhesion sites, integrins connect the extracellular matrix (ECM) with the F-actin cytoskeleton and transduce mechanical forces generated by the actin retrograde flow and myosin II to the ECM through mechanosensitive focal adhesion proteins that are collectively termed the “molecular clutch.” The transmission of forces across integrin-based adhesions establishes a mechanical reciprocity between the viscoelasticity of the ECM and the cellular tension. During mechanotransduction, force allosterically alters the functions of mechanosensitive proteins within adhesions to elicit biochemical signals that regulate both rapid responses in cellular mechanics and long-term changes in gene expression. Integrin-mediated mechanotransduction plays important roles in development and tissue homeostasis, and its dysregulation is often associated with diseases.
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44

Kosoff, David, Jiaquan Yu, Vikram Suresh, David J. Beebe, and Joshua M. Lang. "Surface topography and hydrophilicity regulate macrophage phenotype in milled microfluidic systems." Lab on a Chip 18, no. 19 (2018): 3011–17. http://dx.doi.org/10.1039/c8lc00431e.

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45

Shimamoto, Yuta, Sachiko Tamura, Hiroshi Masumoto, and Kazuhiro Maeshima. "Nucleosome–nucleosome interactions via histone tails and linker DNA regulate nuclear rigidity." Molecular Biology of the Cell 28, no. 11 (June 2017): 1580–89. http://dx.doi.org/10.1091/mbc.e16-11-0783.

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Cells, as well as the nuclei inside them, experience significant mechanical stress in diverse biological processes, including contraction, migration, and adhesion. The structural stability of nuclei must therefore be maintained in order to protect genome integrity. Despite extensive knowledge on nuclear architecture and components, however, the underlying physical and molecular mechanisms remain largely unknown. We address this by subjecting isolated human cell nuclei to microneedle-based quantitative micromanipulation with a series of biochemical perturbations of the chromatin. We find that the mechanical rigidity of nuclei depends on the continuity of the nucleosomal fiber and interactions between nucleosomes. Disrupting these chromatin features by varying cation concentration, acetylating histone tails, or digesting linker DNA results in loss of nuclear rigidity. In contrast, the levels of key chromatin assembly factors, including cohesin, condensin II, and CTCF, and a major nuclear envelope protein, lamin, are unaffected. Together with in situ evidence using living cells and a simple mechanical model, our findings reveal a chromatin-based regulation of the nuclear mechanical response and provide insight into the significance of local and global chromatin structures, such as those associated with interdigitated or melted nucleosomal fibers.
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46

Harada, Mutsuo, and Haruhiro Toko. "Does Mechanical Stress Regulate the Angiogenic Profile of Endothelial Progenitor Cells?" International Heart Journal 57, no. 3 (2016): 268–70. http://dx.doi.org/10.1536/ihj.16-168.

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47

Thorpe, Stephen D., Conor T. Buckley, Fergal J. O'Brien, Anthony J. Robinson, and Daniel J. Kelly. "FABRICATION METHODOLOGIES REGULATE THE INITIAL MECHANICAL PROPERTIES OF CELL SEEDED HYDROGELS." Journal of Biomechanics 41 (July 2008): S383. http://dx.doi.org/10.1016/s0021-9290(08)70382-8.

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48

Bleuel, Judith, Frank Zaucke, Nina Hamann, Gert-Peter Brüggemann, and Anja Niehoff. "MECHANICAL SIGNALS REGULATE THE ANCHORAGE OF COMP IN THE CHONDROCYTE MATRIX." Journal of Biomechanics 45 (July 2012): S434. http://dx.doi.org/10.1016/s0021-9290(12)70435-9.

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49

Liu, Chao, Xin Cui, Thomas M. Ackermann, Vittoria Flamini, Weiqiang Chen, and Alesha B. Castillo. "Osteoblast-derived paracrine factors regulate angiogenesis in response to mechanical stimulation." Integrative Biology 8, no. 7 (2016): 785–94. http://dx.doi.org/10.1039/c6ib00070c.

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50

Sharp, W. W., D. G. Simpson, T. K. Borg, A. M. Samarel, and L. Terracio. "Mechanical forces regulate focal adhesion and costamere assembly in cardiac myocytes." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 2 (August 1, 1997): H546—H556. http://dx.doi.org/10.1152/ajpheart.1997.273.2.h546.

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To determine whether the formation and maintenance of focal adhesions and costameres in cardiac myocytes are influenced by the mechanical forces that they transmit, we mechanically unloaded these cells by inhibiting their spontaneous contractile activity with the calcium-channel blocker nifedipine (12 microM). Interference-reflection and fluorescence microscopy revealed that within 24 h of arrest, beta 1-integrin- and vinculin-positive focal adhesions and costameres were disrupted. Loss of mature beta 1-integrin from the cell surface was observed in cell surface-labeling experiments and in Western blots. Subjecting nonbeating cells to a 5% static stretch for 24 h resulted in an increase of 21% for beta 1-integrin and 39% for vinculin. Stretching beating cells resulted in 71 and 9% increases, respectively. Intracellular concentrations of pre-beta 1 were not affected by contractile activity or by stretch. Our results indicate that mechanical forces stabilize the cellular levels of beta 1-integrin and vinculin by possibly regulating their association with the formation and maintenance of focal adhesions and costameres.
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