Monte carlo simulation of heterotypic cell aggregation in nonlinear shear flow

Wang, Jiakou; Slattery, Margaret J.; Hoskins, Meghan H.; Liang, Shuang; Dong, Chuan; Du, Qiang

doi:10.3934/mbe.2006.3.683

Cited by 11 publications

(8 citation statements)

References 26 publications

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“…In studies by Wang et al 31 33 introduced a 3-dimensional thrombus formation model. Each platelet is treated as a spherical object, and the suspension of red blood cells is treated as a continuum.…”

Section: Integrated Thrombogenesis Modelsmentioning

confidence: 99%

Computational Approaches to Studying Thrombus Development

Kamocka

Alber

et al. 2011

ATVB

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Abstract-In addition to descriptive biological models, many computational models have been developed for hemostasis/ thrombosis that provide quantitative characterization of thrombus development. Simulations using computational models that have been developed for coagulation reactions, platelet activation, and fibrinogen assembly have been shown to be in close agreement with experimental data. Models of processes involved in hemostasis/thrombosis are being integrated to simulate the development of the thrombus simultaneously in time and space. Key Words: blood coagulation Ⅲ blood flow Ⅲ coagulation Ⅲ platelets Ⅲ thrombosis Ⅲ computational model Ⅲ stochastic multiscale model Ⅲ thrombus development S ignificant progress has been made in our understanding of the hemostatic response. For instance, coagulation pathways 1 have been developed that describe the interactions among different elements and provide insight into the regulation of the response. Similarly, advances in platelet biology 2 have elucidated pathways of platelet activation and identified and characterized molecular components involved in intracellular signaling, as well as surface proteins mediating adhesion to the damaged vessel wall, to other platelets, and to other thrombus components. Furthermore, the development of transgenic, 3,4 gene knockout, and gene knock-in technologies has enabled exploration of the physiological roles of individual components in vivo using sophisticated hemostatic experimental systems. More recently, genomic and proteomic approaches have identified new elements modifying the hemostatic response.The initial identification of hemostatic components and description of coagulation or platelet signaling pathways were qualitative, 4,5 describing the order of interaction among components in coagulation or platelet behavior. These biological and biochemical models were extremely valuable, suggesting how these processes might be regulated and providing an understanding of how deficiencies or dysregulation of particular components leads to pathological states.In addition to these descriptive biological models, computational models have been developed for hemostatic processes that provide quantitative characterization of thrombus development. For instance, the tissue factor (TF)-initiated coagulation model introduced by Hockin et al 6 presented a quantitative description of the network of coagulation reactions. The model correctly predicted that there was a TF concentration threshold required to activate the coagulation system to generate the thrombin required for a hemostatic response. In addition, the computational model introduced by Purvis et al 7 to simulate ADP-mediated platelet activation provided insight into possible mechanisms of negativefeedback signaling and cell-to-cell variation across platelet populations. Furthermore, the kinetic model of fibrin polymerization introduced by Weisel and Nagaswami 8 revealed that changes in the rate of fibrinopeptide cleavage were sufficient to explain many nonintuitive experimental obs...

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Section: Integrated Thrombogenesis Modelsmentioning

confidence: 99%

Computational Approaches to Studying Thrombus Development

Kamocka

Alber

et al. 2011

ATVB

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“…(40) Also, our previous work has shown that melanoma deformability enhances adhesion to endothelial cells under shear flow by increasing contact area. (41; 42)…”

Section: Discussionmentioning

confidence: 99%

Nuclear Stiffening Inhibits Migration of Invasive Melanoma Cells

Ribeiro¹,

Khanna

Sukumar³

et al. 2014

Cel. Mol. Bioeng.

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During metastasis, melanoma cells must be sufficiently deformable to squeeze through extracellular barriers with small pore sizes. We visualize and quantify deformability of single cells using micropipette aspiration and examine the migration potential of a population of melanoma cells using a flow migration apparatus. We artificially stiffen the nucleus with recombinant overexpression of Δ50 lamin A, which is found in patients with Hutchison Gilford progeria syndrome and in aged individuals. Melanoma cells, both WM35 and Lu1205, both show reduced nuclear deformability and reduced cell invasion with the expression of Δ50 lamin A. These studies suggest that cellular aging including expression of Δ50 lamin A and nuclear stiffening may reduce the potential for metastatic cancer migration. Thus, the pathway of cancer metastasis may be kept in check by mechanical factors in addition to known chemical pathway regulation.

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“…We hypothesize that statistical model-of-model approaches can be brought to bear, thereby reducing compute times by many orders of magnitude compared to direct scaling to the cell-population. Other workers have proposed population balance and stochastic aggregation methods for coagulation and heterotypic cell adhesion and aggregation [57][58][59]. These methods are both appropriate-for and limited-to aggregation processes.…”

Section: Adhesion Biochemistrymentioning

confidence: 98%

Multi-scale biological and physical modelling of the tumour micro-environment

Kunz

Gaskin

et al. 2015

Drug Discovery Today: Disease Models

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Paced by advances in high performance computing, and algorithms for multi-physics and multi-scale simulation, a number of groups have recently established numerical models of flowing blood systems, where cellscale interactions are explicitly resolved. To be biologically representative, these models account for some or all of: (1) fluid dynamics of the carrier flow, (2) structural dynamics of the cells and vessel walls, (3) interaction and transport biochemistry, and, (4) methods for scaling to physiologically representative numbers of cells. In this article, our interest is the modelling of the tumour micro-environment. We review the broader area of cell-scale resolving blood flow modelling, while focusing on the particular interactions of tumour cells and white blood cells, known to play an important role in metastasis.

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Monte carlo simulation of heterotypic cell aggregation in nonlinear shear flow

Cited by 11 publications

References 26 publications

Computational Approaches to Studying Thrombus Development

Computational Approaches to Studying Thrombus Development

Nuclear Stiffening Inhibits Migration of Invasive Melanoma Cells

Multi-scale biological and physical modelling of the tumour micro-environment

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