Macrophage adhesion on fibronectin evokes an increase in the elastic property of the cell membrane and cytoskeleton: an atomic force microscopy study

Souza, Samuel T.; Agra, Laís Costa; Santos, Cássio Eráclito Alves dos; Barreto, Emiliano; Hickmann, Jandir M.; Fonseca, E. J. S.

doi:10.1007/s00249-014-0988-3

Cited by 24 publications

(16 citation statements)

References 41 publications

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“…Muscle fiber protein production decreases in the absence of mechanical stimulation [ 63 ], and protein breakdown transiently increases then diminishes during disuse [ 63 ]; both of these responses are dependent on muscle fiber type [ 64 ]. Furthermore, many non-muscle fiber cells are also sensitive to the mechanical environment in muscle [ 65 – 67 ]. For example, fibroblasts are affected by changes in mechanical stimulation which alters their production of ECM [ 68 ], and affects their proliferation [ 69 , 70 ], apoptosis [ 71 ], and growth factor secretion [ 72 ].…”

Section: Muscle Has a Mind Of Its Own: A Computational Framework To Mmentioning

confidence: 99%

Skeletal muscle mechanics, energetics and plasticity

Lieber

Roberts

Blemker

et al. 2017

J NeuroEngineering Rehabil

114

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The following papers by Richard Lieber (Skeletal Muscle as an Actuator), Thomas Roberts (Elastic Mechanisms and Muscle Function), Silvia Blemker (Skeletal Muscle has a Mind of its Own: a Computational Framework to Model the Complex Process of Muscle Adaptation) and Sabrina Lee (Muscle Properties of Spastic Muscle (Stroke and CP) are summaries of their representative contributions for the session on skeletal muscle mechanics, energetics and plasticity at the 2016 Biomechanics and Neural Control of Movement Conference (BANCOM 2016). Dr. Lieber revisits the topic of sarcomere length as a fundamental property of skeletal muscle contraction. Specifically, problems associated with sarcomere length non-uniformity and the role of sarcomerogenesis in diseases such as cerebral palsy are critically discussed. Dr. Roberts then makes us aware of the (often neglected) role of the passive tissues in muscles and discusses the properties of parallel elasticity and series elasticity, and their role in muscle function. Specifically, he identifies the merits of analyzing muscle deformations in three dimensions (rather than just two), because of the potential decoupling of the parallel elastic element length from the contractile element length, and reviews the associated implications for the architectural gear ratio of skeletal muscle contraction. Dr. Blemker then tackles muscle adaptation using a novel way of looking at adaptive processes and what might drive adaptation. She argues that cells do not have pre-programmed behaviors that are controlled by the nervous system. Rather, the adaptive responses of muscle fibers are determined by sub-cellular signaling pathways that are affected by mechanical and biochemical stimuli; an exciting framework with lots of potential. Finally, Dr. Lee takes on the challenging task of determining human muscle properties in vivo. She identifies the dilemma of how we can demonstrate the effectiveness of a treatment, specifically in cases of muscle spasticity following stroke or in children with cerebral palsy. She then discusses the merits of ultrasound based elastography, and the clinical possibilities this technique might hold. Overall, we are treated to a vast array of basic and clinical problems in skeletal muscle mechanics and physiology, with some solutions, and many suggestions for future research.

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Section: Muscle Has a Mind Of Its Own: A Computational Framework To Mmentioning

confidence: 99%

Skeletal muscle mechanics, energetics and plasticity

Lieber

Roberts

Blemker

et al. 2017

J NeuroEngineering Rehabil

114

View full text Add to dashboard Cite

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“…Cell adhesion is essential to cellular functions such as survival, exocytosis, differentiation, cell-cell communication and signal transduction, which evokes a variety of biophysical changes in cellular organization, including modification of the cytoskeleton and plasma membrane (Souza et al, 2014). The adhesion force can be obtained from the AFM retract force-distance curves.…”

Section: Changes In Nanomechanical Properties and Cytoskeletal Proteimentioning

confidence: 99%

Detection of CD28/CD86 co‐stimulatory molecules and surface properties of T and dendritic cells: An AFM study

et al. 2015

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Although the importance of B7/CD28 co-stimulation has been widely studied, little is known about their nano-spatial localization and their corresponding cells' biophysical and biomechanical properties. Here, we investigated the morphological, biophysical, and biomechanical properties of T cells and dendritic cells (DCs) by atomic force microscopy (AFM) and force curves. The nano-spatial distribution of CD28 and CD86 antigen on T cells and DCs was detected by CD86 or CD28 antibody-functionalized AFM tip. Single-molecule force spectroscopy (SMFS)-based force volumes and quantum dots (QDs)-based fluorescence imaging demonstrated that the co-stimulatory molecules were not randomly distributed over the cells' surface, but more than 80% of CD28 and CD86 molecules appeared to be expressed as 100-200 nm nanoclusters and polarize dominantly in the peak of the cell membrane fluctuations. AFM imaging and quantitative analysis showed that the roughness of mature DCs (mDCs) was higher than that of immature DCs (iDCs). The adhesion force distribution of iDCs and mDCs was heterogeneous while the elasticity distribution was homogeneous locally. In addition, mDCs had a fourfold increase of Young's modulus of iDCs, indicating the contribution of the actin cytoskeleton to the elastic properties of the cells. Taken together, the nano-cluster distribution of CD28 and CD86, the rough mDCs surface, the higher adhesion force and elasticity of mDCs may facilitate to the occurrence of B7/CD28 co-stimulation signals and the formation of immune synapse. These nanoscale findings provide new insights into the antigen-presenting function of DCs, the T cell activation and ultimate immune response. SCANNING 38:365-375, 2016. © 2015 Wiley Periodicals, Inc.

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“…Muscle fiber protein production decreases in the absence of mechanical stimulation (46), and protein breakdown transiently increases then diminishes during disuse (46); both of these responses are likely dependent on muscle fiber type (72). Furthermore, many nonmuscle fiber cells are also sensitive to the mechanical environment in muscle (15,19,56,60,62). For instance, fibroblasts are affected by changes in mechanical stimulation, which alters their production of extracellular matrix (ECM) (66) and affects their proliferation (54,76), apoptosis (59), and growth factor secretion (58).…”

mentioning

confidence: 99%

Agent-based computational model investigates muscle-specific responses to disuse-induced atrophy

Martin

Blemker

Peirce

2015

Journal of Applied Physiology

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Martin KS, Blemker SS, Peirce SM. Agent-based computational model investigates muscle-specific responses to disuse-induced atrophy. J Appl Physiol 118: 1299 -1309, 2015. First published February 26, 2015 doi:10.1152/japplphysiol.01150.2014.-Skeletal muscle is highly responsive to use. In particular, muscle atrophy attributable to decreased activity is a common problem among the elderly and injured/ immobile. However, each muscle does not respond the same way. We developed an agent-based model that generates a tissue-level skeletal muscle response to disuse/immobilization. The model incorporates tissue-specific muscle fiber architecture parameters and simulates changes in muscle fiber size as a result of disuse-induced atrophy that are consistent with published experiments. We created simulations of 49 forelimb and hindlimb muscles of the rat by incorporating eight fiber-type and size parameters to explore how these parameters, which vary widely across muscles, influence sensitivity to disuse-induced atrophy. Of the 49 muscles modeled, the soleus exhibited the greatest atrophy after 14 days of simulated immobilization (51% decrease in fiber size), whereas the extensor digitorum communis atrophied the least (32%). Analysis of these simulations revealed that both fibertype distribution and fiber-size distribution influence the sensitivity to disuse atrophy even though no single tissue architecture parameter correlated with atrophy rate. Additionally, software agents representing fibroblasts were incorporated into the model to investigate cellular interactions during atrophy. Sensitivity analyses revealed that fibroblast agents have the potential to affect disuse-induced atrophy, albeit with a lesser effect than fiber type and size. In particular, muscle atrophy elevated slightly with increased initial fibroblast population and increased production of TNF-␣. Overall, the agent-based model provides a novel framework for investigating both tissue adaptations and cellular interactions in skeletal muscle during atrophy. agent-based model; muscle atrophy; fiber type; tissue architecture; fibroblasts SKELETAL MUSCLE ADAPTS to activity levels, where elevated activity leads to increases in muscle size (muscle hypertrophy) and diminished activity levels lead to decreases in muscle size (muscle atrophy) (6, 36).1 Muscle atrophy is estimated to affect 45% of the U.S. elderly population and directly attributed to 1.5% of total direct healthcare costs in 2000 ($18.5 billion) (25). In young people, diminished activity as a consequence of surgery-related immobilization (2, 68), bed rest (33), or long-term mechanical ventilation (34) lead to disabling muscle weakness.Muscle atrophy, triggered by loss of mechanical stimulation, causes changes in the behavior of the various cell types that comprise muscle tissue (52, 53). Muscle fiber protein production decreases in the absence of mechanical stimulation (46), and protein breakdown transiently increases then diminishes during disuse (46); both of these responses are likely dependent ...

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Macrophage adhesion on fibronectin evokes an increase in the elastic property of the cell membrane and cytoskeleton: an atomic force microscopy study

Cited by 24 publications

References 41 publications

Skeletal muscle mechanics, energetics and plasticity

Skeletal muscle mechanics, energetics and plasticity

Detection of CD28/CD86 co‐stimulatory molecules and surface properties of T and dendritic cells: An AFM study

Agent-based computational model investigates muscle-specific responses to disuse-induced atrophy

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