Collective Cell Migration in 3D Epithelial Wound Healing

ACS Nano ◽  
2019 ◽  
Author(s):  
Yuan Xiao ◽  
Reza Riahi ◽  
Peter Torab ◽  
Donna D. Zhang ◽  
Pak Kin Wong
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Collective Cell Migration ◽  
Epithelial Wound Healing

Quantitative Imaging of pN Intercellular Force and Energetic Costs during Collective Cell Migration in Epithelial Wound Healing

2020 ◽  
Vol 92 (24) ◽  
pp. 16180-16187
Author(s):  
Xiao-Hong Wang ◽  
Fan Yang ◽  
Jian-Bin Pan ◽  
Bin Kang ◽  
Jing-Juan Xu ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Quantitative Imaging ◽  
Collective Cell Migration ◽  
Energetic Costs ◽  
Epithelial Wound Healing

scholarly journals Hierarchical modeling of mechano-chemical dynamics of epithelial sheets across cells and tissue

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yoshifumi Asakura ◽  
Yohei Kondo ◽  
Kazuhiro Aoki ◽  
Honda Naoki
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Continuum Model ◽  
Tissue Level ◽  
Chemical Signals ◽  
Cellular Level ◽  
Mathematical Framework ◽  
Collective Cell Migration ◽  
The Continuum ◽  
Cell Cell

AbstractCollective cell migration is a fundamental process in embryonic development and tissue homeostasis. This is a macroscopic population-level phenomenon that emerges across hierarchy from microscopic cell-cell interactions; however, the underlying mechanism remains unclear. Here, we addressed this issue by focusing on epithelial collective cell migration, driven by the mechanical force regulated by chemical signals of traveling ERK activation waves, observed in wound healing. We propose a hierarchical mathematical framework for understanding how cells are orchestrated through mechanochemical cell-cell interaction. In this framework, we mathematically transformed a particle-based model at the cellular level into a continuum model at the tissue level. The continuum model described relationships between cell migration and mechanochemical variables, namely, ERK activity gradients, cell density, and velocity field, which could be compared with live-cell imaging data. Through numerical simulations, the continuum model recapitulated the ERK wave-induced collective cell migration in wound healing. We also numerically confirmed a consistency between these two models. Thus, our hierarchical approach offers a new theoretical platform to reveal a causality between macroscopic tissue-level and microscopic cellular-level phenomena. Furthermore, our model is also capable of deriving a theoretical insight on both of mechanical and chemical signals, in the causality of tissue and cellular dynamics.

scholarly journals Viscoelasticity and cell jamming state transition

2021 ◽  
Author(s):  
Ivana Pajic-Lijakovic ◽  
Milan Milivojevic
Keyword(s):  
Residual Stress ◽  
Wound Healing ◽  
Cell Migration ◽  
State Transition ◽  
State Transitions ◽  
Collective Cell Migration ◽  
Biological Processes ◽  
Cell Mobility ◽  
Controversial Topic ◽  
The Impact

Although collective cell migration (CCM) is a highly coordinated migratory mode, perturbations in the form of jamming state transitions and vice versa often occur even in 2D. These perturbations are involved in various biological processes, such as embryogenesis, wound healing and cancer invasion. CCM induces accumulation of cell residual stress which has a feedback impact to cell packing density. Density-mediated change of cell mobility influences the state of viscoelasticity of multicellular systems and on that base the jamming state transition. Although a good comprehension of how cells collectively migrate by following molecular rules has been generated, the impact of cellular rearrangements on cell viscoelasticity remains less understood. Thus, considering the density driven evolution of viscoelasticity caused by reduction of cell mobility could result in a powerful tool in order to address the contribution of cell jamming state transition in CCM and help to understand this important but still controversial topic. In addition, five viscoelastic states gained within three regimes: (1) convective regime, (2) conductive regime, and (3) damped-conductive regime was discussed based on the modeling consideration with special emphasis of jamming and unjamming states.

scholarly journals A Role for the Mitogen-activated Protein Kinase Kinase Kinase 1 in Epithelial Wound Healing

2006 ◽  
Vol 17 (8) ◽  
pp. 3446-3455 ◽  
Author(s):  
Maoxian Deng ◽  
Wei-Li Chen ◽  
Atsushi Takatori ◽  
Zhimin Peng ◽  
Lin Zhang ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Epithelial Cell ◽  
Skin Wound ◽  
Mitogen Activated Protein Kinase ◽  
Epithelial Cell Migration ◽  
Epithelial Wound Healing ◽  
Mitogen Activated Protein ◽  
Pai 1 ◽  
Protein Kinase Kinase

The mitogen-activated protein kinase kinase (MEK) kinase 1 (MEKK1) mediates activin B signals required for eyelid epithelium morphogenesis during mouse fetal development. The present study investigates the role of MEKK1 in epithelial wound healing, another activin-regulated biological process. In a skin wound model, injury markedly stimulates MEKK1 expression and activity, which are in turn required for the expression of genes involved in extracellular matrix (ECM) homeostasis. MEKK1 ablation or down-regulation by interfering RNA significantly delays skin wound closure and impairs activation of Jun NH2-terminal kinases, induction of plasminogen activator inhibitor (PAI)-1, and restoration of cell–cell junctions of the wounded epidermis. Conversely, expression of wild-type MEKK1 accelerates reepithelialization of full-thickness skin and corneal debridement wounds by mechanisms involving epithelial cell migration, a cell function that is partially abolished by neutralizing antibodies for PAI-1 and metalloproteinase III. Our data suggest that MEKK1 transmits wound signals, leading to the transcriptional activation of genes involved in ECM homeostasis, epithelial cell migration, and wound reepithelialization.

scholarly journals Fingering instability in spreading epithelial monolayers: roles of cell polarisation, substrate friction and contractile stresses

Soft Matter ◽  
2021 ◽  
Author(s):  
Carolina Trenado ◽  
Luis L. Bonilla ◽  
Alejandro Martínez-Calvo
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Cancer Progression ◽  
Coherent Structures ◽  
Crucial Role ◽  
Collective Cell Migration ◽  
Developmental Processes ◽  
Epithelial Monolayers ◽  
Fingering Instability

Collective cell migration plays a crucial role in many developmental processes that underlie morphogenesis, wound healing, or cancer progression. In such coordinated behaviours, cells are organised in coherent structures and...

Mechanisms of Collective Cell Migration in Wound Healing: Physiology and Disease

2021 ◽  
pp. 55-74
Author(s):  
Chaithra Mayya ◽  
Sumit Kharbhanda ◽  
Ashadul Haque ◽  
Dhiraj Bhatia
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Collective Cell Migration

scholarly journals Rho kinases regulate corneal epithelial wound healing

2008 ◽  
Vol 295 (2) ◽  
pp. C378-C387 ◽  
Author(s):  
Jia Yin ◽  
Fu-Shin X. Yu
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Cell Migration ◽  
Rho Gtpase ◽  
Adhesion Formation ◽  
Small Gtpase ◽  
Corneal Epithelial Cell ◽  
Corneal Epithelial ◽  
Epithelial Wound Healing ◽  
Rho Kinases

We have previously shown that Rho small GTPase is required for modulating both cell migration and proliferation through cytoskeleton reorganization and focal adhesion formation in response to wounding. In the present study, we investigated the role of Rho kinases (ROCKs), major effectors of Rho GTPase, in mediating corneal epithelial wound healing. Both ROCK 1 and 2 were expressed and activated in THCE cells, an SV40-immortalized human corneal epithelial cell (HCEC) line, in response to wounding, lysophosphatidic acid, and heparin-binding EGF-like growth factor (HB-EGF) stimulations. The ROCK inhibitor Y-27632 efficiently antagonized ROCK activities without affecting Rho activation in wounded HCECs. Y-27632 promoted basal and HB-EGF-enhanced scratch wound healing and enhanced cell migration and adhesion to matrices, while retarded HB-EGF induced cell proliferation. E-cadherin- and β-catenin-mediated cell-cell junction and actin cytoskeleton organization were disrupted by Y-27632. Y-27632 impaired the formation and maintenance of tight junction barriers indicated by decreased trans-epithelial resistance and disrupted occludin staining. We conclude that ROCK activities enhance cell proliferation, promote epithelial differentiation, but negatively modulate cell migration and cell adhesion and therefore play a role in regulating corneal epithelial wound healing.

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