Physical view on migration modes

Mierke, Claudia Tanja

doi:10.1080/19336918.2015.1066958

Cited by 33 publications

(28 citation statements)

References 150 publications

(125 reference statements)

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“…In vivo migration of cells generally occurs under fluid flow in blood vessels or interstitial cavities through metastasis of cancer cells, [1] immune response [2], embryonic development [3], and tissue regeneration [4]. A large number of in vitro studies basing on microfluidic technology or parallel-plate flow chamber were performed to investigate the effect of fluid shear stress (FSS) on cell migration.…”

Section: Introductionmentioning

confidence: 99%

Gradient fluid shear stress regulates migration of osteoclast precursors

Gao

Sun

et al. 2019

Cell Adhesion & Migration

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Cell migration is highly sensitive to fluid shear stress (FSS) in blood flow or interstitial fluid flow. However, whether the FSS gradient can regulate the migration of cells remains unclear. In this work, we constructed a parallel-plate flow chamber with different FSS gradients and verified the gradient flow field by particle image velocimetry measurements and finite element analyses. We then investigated the effect of FSS magnitudes and gradients on the migration of osteoclast precursor RAW264.7 cells. Results showed that the cells sensed the FSS gradient and migrated toward the low-FSS region. This FSS gradient-induced migration tended to occur in low-FSS magnitudes and high gradients, e.g., the migration angle relative to flow direction was approximately 90° for 0.1 Pa FSS and 0.2 Pa mm −1 FSS gradient. When chemically inhibiting the calcium signaling pathways of the mechanosensitive cation channel, endoplasmic reticulum, phospholipase C, and extracellular calcium, the cell migration toward the low-FSS region was significantly reduced. This study may provide insights into the mechanism of the recruitment of osteoclast precursors at the site of bone resorption and of mechanical stimulation-induced bone remodeling.

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Section: Introductionmentioning

confidence: 99%

Gradient fluid shear stress regulates migration of osteoclast precursors

Gao

Sun

et al. 2019

Cell Adhesion & Migration

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“…This mechanism is mediated by the Akt/NF-κB pathway: the undecapeptide increases tumor-associated cytokines and NF-κB p65 expression and decreases cancer cell proliferation/migration when a reduced activation of Akt/NF-κB occurs [38]. The SP/NK-1R system also controls membrane blebbing, a mechanism related to cell migration and spreading [29,38,59,60]. Moreover, SP favors the expression of matrix metalloproteinases (degradative enzymes) by enhancing the activation of several signaling pathways (Akt, JNK, ERK1/2) and promoting cancer Preprints (www.preprints.org) | NOT PEER-REVIEWED | Posted: 14 April 2020 doi:10.20944/preprints202004.0224.v1 5 of 21 cell migration, invasion and metastasis [61,62], processes that are inhibited by NK-1R antagonists [38].…”

Section: The Sp/nk-1r System and Cancer: Cell Signaling Pathways Ovementioning

confidence: 99%

The Neurokinin-1 Receptor Antagonist Aprepitant, a New Drug for the Treatment of Hematological Malignancies: Focus on Acute Myeloid Leukemia

Muñoz

Coveñas

2020

Preprint

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Acute myeloid leukemia (AML) is an incurable hematological malignancy. To treat the disease successfully, new therapeutic strategies are urgently needed. One of these strategies can be the use of neurokinin-1 receptor (NK-1R) antagonists (e.g., aprepitant), because the substance P (SP)/NK-1R system is involved in cancer progression, including AML. AML patients show an up-regulation of the NK-1R mRNA expression; human AML cell lines show immunoreactivity for both SP and the NK-1R (it is overexpressed: the truncated isoform is more expressed than the full-length form) and, via this receptor, SP and NK-1R antagonists (aprepitant, in a concentration-dependent manner) respectively exert a proliferative action or an antileukemic effect (apoptotic mechanisms are triggered by promoting oxidative stress via mitochondrial Ca ++ overload). Aprepitant inhibits the formation of AML cell colonies and, in combination with chemotherapeutic drugs, is more effective in inducing cytotoxic effects and AML cell growth blockade. NK-1R antagonists also exert an antinociceptive effect in myeloid leukemia-induced bone pain. The antitumor effect of aprepitant is diminished when the NF-κB pathway is overactivated and the damage induced by aprepitant in cancer cells is higher than that exerted in non-cancer cells.Thus, the SP/NK-1R system is involved in AML and aprepitant is a promising antitumor strategy against this hematological malignancy. In this review, the involvement of this system in solid and non-solid tumors (in particular in AML) is up-dated and the use of aprepitant as an anti-leukemic strategy for the treatment of AML is also mentioned (a dose of aprepitant (> 20 mg/kg/day) for a period of time according to the response to treatment is suggested).

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“…While cell migration on 2D substrates is well characterized, the subcellular processes underlying 3D cell migration and their dependency on the physical properties of the ECM are less understood. Reported cell migration modes range from bleb-based to protrusion-based [3]. In the former, intracellular pressure results in membrane expulsions called blebs that form without actin polymerization [4].…”

Section: Introductionmentioning

confidence: 99%

The role of actin protrusion dynamics in cell migration through a degradable viscoelastic extracellular matrix: Insights from a computational model

et al. 2020

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Actin protrusion dynamics plays an important role in the regulation of three-dimensional (3D) cell migration. Cells form protrusions that adhere to the surrounding extracellular matrix (ECM), mechanically probe the ECM and contract in order to displace the cell body. This results in cell migration that can be directed by the mechanical anisotropy of the ECM. However, the subcellular processes that regulate protrusion dynamics in 3D cell migration are difficult to investigate experimentally and therefore not well understood. Here, we present a computational model of cell migration through a degradable viscoelastic ECM. This model is a 2D representation of 3D cell migration. The cell is modeled as an active deformable object that captures the viscoelastic behavior of the actin cortex and the subcellular processes underlying 3D cell migration. The ECM is regarded as a viscoelastic material, with or without anisotropy due to fibrillar strain stiffening, and modeled by means of the meshless Lagrangian smoothed particle hydrodynamics (SPH) method. ECM degradation is captured by local fluidization of the material and permits cell migration through the ECM. We demonstrate that changes in ECM stiffness and cell strength affect cell migration and are accompanied by changes in number, lifetime and length of protrusions. Interestingly, directly changing the total protrusion number or the average lifetime or length of protrusions does not affect cell migration. A stochastic variability in protrusion lifetime proves to be enough to explain differences in cell migration velocity. Force-dependent adhesion disassembly does not result in faster migration, but can make migration more efficient. We also demonstrate that when a number of simultaneous protrusions is enforced, the optimal number of simultaneous protrusions is one or two, depending on ECM anisotropy. Together, the model provides non-trivial new insights in the role of protrusions in 3D cell migration and can be a valuable contribution to increase the understanding of 3D cell migration mechanics.PLOS Computational Biology | https://doi.The ability of cells to migrate through a tissue in the human body is vital for many processes such as tissue development, growth and regeneration. At the same time, abnormal cell migration is also playing an important role in many diseases such as cancer. If we want to be able to explain the origin of these abnormalities and develop new treatment strategies, we have to understand how cells are able to regulate their migration. Since it is challenging to investigate cell migration through a biological tissue in experiments, computational modeling can provide a valuable contribution. We have developed a computational model of cell migration through a deformable and degradable material that describes both mechanics of the cell and the surrounding material and subcellular processes underlying cell migration. This model captures the formation of long and thin protrusions that adhere to the surrounding material and that pull the cell forward. I...

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Physical view on migration modes

Cited by 33 publications

References 150 publications

Gradient fluid shear stress regulates migration of osteoclast precursors

Gradient fluid shear stress regulates migration of osteoclast precursors

The Neurokinin-1 Receptor Antagonist Aprepitant, a New Drug for the Treatment of Hematological Malignancies: Focus on Acute Myeloid Leukemia

The role of actin protrusion dynamics in cell migration through a degradable viscoelastic extracellular matrix: Insights from a computational model

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