Cooperative contractility: The role of stress fibres in the regulation of cell-cell junctions

Ronan, William; McMeeking, Robert M.; Chen, Christopher; McGarry, J. Patrick; Deshpande, V.S.

doi:10.1016/j.jbiomech.2014.11.025

Cited by 14 publications

(4 citation statements)

References 32 publications

(45 reference statements)

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“…Upon exposure to TDNs, chondrocytes may send complicated biological signals to make adjustments of microtubules and the expression of relevant genes. Computational models have revealed that cellular microtubule compression force may influence stress fibers . Therefore, after 24 h of exposure to TDNs, chondrocytes displayed a relevant round morphology, which is similar to the chondrocyte phenotype and what is more, the relevant genes related to the Notch signaling pathway was downregulated.…”

Section: Resultsmentioning

confidence: 99%

Tetrahedral DNA Nanostructure: A Potential Promoter for Cartilage Tissue Regeneration via Regulating Chondrocyte Phenotype and Proliferation

Shao

Lin

Peng

et al. 2017

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124

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Utilizing biomaterials to regulate the phenotype and proliferation of chondrocytes is a promising approach for effective cartilage tissue regeneration. Recently, a significant amount of effort has been invested into directing chondrocytes toward a desired location and function by utilizing biomaterials to control the dedifferentiation and phenotypic loss of chondrocytes during in vitro monolayer culture. Here, the transmission signals resulting from tetrahedral DNA nanostructures (TDNs) in the regulation of chondrocyte phenotype and proliferation are exploited. TDNs, new DNA nanomaterials, have been considered as promising materials in biomedical fields. Upon exposure to TDNs, chondrocyte phenotype is significantly enhanced, accompanied by lower gene expression related to Notch signaling pathway and higher expression of type II collagen. In addition, the cell proliferation and morphology of chondrocytes are changed after exposure to TDNs. In conclusion, this work demonstrates that TDNs are potentially useful mechanism in cartilage tissue regeneration from chondrocytes, whereby chondrocyte phenotype and proliferation can be retained.

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Section: Resultsmentioning

confidence: 99%

Tetrahedral DNA Nanostructure: A Potential Promoter for Cartilage Tissue Regeneration via Regulating Chondrocyte Phenotype and Proliferation

Shao

Lin

Peng

et al. 2017

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124

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“…Previous work has shown that the elastic modulus of MSCs is significantly influenced by the cytoskeleton (Titushkin and Cho, 2007). Adhesion junctions transmit mechanical forces such as cytoskeletal tension between cells (Ganz et al, 2006; Maruthamuthu et al, 2011) and are strengthened and stabilised by interaction with the cytoskeleton (Pittet et al, 2008; Liu et al, 2010; Hong et al, 2013; Ronan et al, 2015). In this study we demonstrate that the cytoskeleton/adhesion junction relationship is reciprocal; adhesion junctions also influence stress fibre formation and mesensphere mechanical behaviour.…”

Section: Discussionmentioning

confidence: 99%

The role of adhesion junctions in the biomechanical behaviour and osteogenic differentiation of 3D mesenchymal stem cell spheroids

Griffin

Schiavi

McDevitt

et al. 2017

Journal of Biomechanics

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Osteogenesis of mesenchymal stem cells (MSC) can be regulated by the mechanical environment. MSCs grown in 3D spheroids (mesenspheres) have preserved multi-lineage potential, improved differentiation efficiency, and exhibit enhanced osteogenic gene expression and matrix composition in comparison to MSCs grown in 2D culture. Within 3D mesenspheres, mechanical cues are primarily in the form of cell-cell contraction, mediated by adhesion junctions, and as such adhesion junctions are likely to play an important role in the osteogenic differentiation of mesenspheres. However the precise role of N- and OB-cadherin on the biomechanical behaviour of mesenspheres remains unknown. Here we have mechanically tested mesenspheres cultured in suspension using parallel plate compression to assess the influence of N-cadherin and OB-cadherin adhesion junctions on the viscoelastic properties of the mesenspheres during osteogenesis. Our results demonstrate that N-cadherin and OB-cadherin have different effects on mesensphere viscoelastic behaviour and osteogenesis. When OB-cadherin was silenced, the viscosity, initial and long term Young's moduli and actin stress fibre formation of the mesenspheres increased in comparison to N-cadherin silenced mesenspheres and mesenspheres treated with a scrambled siRNA (Scram) at day 2. Additionally, the increased viscoelastic material properties correlate with evidence of calcification at an earlier time point (day 7) of OB-cadherin silenced mesenspheres but not Scram. Interestingly, both N-cadherin and OB-cadherin silenced mesenspheres had higher BSP2 expression than Scram at day 14. Taken together, these results indicate that N-cadherin and OB-cadherin both influence mesensphere biomechanics and osteogenesis, but play different roles.

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“…Upregulation in RhoA activity can initiate high engagement of myosin with actin filaments to yield dense stress fibers, which can promote clustering of cadherin proteins and transmit high tension to cadherin bonds 17 , 18 . Mechanical stress regulates cadherin turnover at cell junctions 19 and directly increases the size of cell-cell adhesions 20 , 21 . RhoA activation has also been shown to induce junction contraction and strengthening 22 , 23 .…”

Section: Introductionmentioning

confidence: 99%

Feedback between mechanosensitive signaling and active forces governs endothelial junction integrity

et al. 2022

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The formation and recovery of gaps in the vascular endothelium governs a wide range of physiological and pathological phenomena, from angiogenesis to tumor cell extravasation. However, the interplay between the mechanical and signaling processes that drive dynamic behavior in vascular endothelial cells is not well understood. In this study, we propose a chemo-mechanical model to investigate the regulation of endothelial junctions as dependent on the feedback between actomyosin contractility, VE-cadherin bond turnover, and actin polymerization, which mediate the forces exerted on the cell-cell interface. Simulations reveal that active cell tension can stabilize cadherin bonds, but excessive RhoA signaling can drive bond dissociation and junction failure. While actin polymerization aids gap closure, high levels of Rac1 can induce junction weakening. Combining the modeling framework with experiments, our model predicts the influence of pharmacological treatments on the junction state and identifies that a critical balance between RhoA and Rac1 expression is required to maintain junction stability. Our proposed framework can help guide the development of therapeutics that target the Rho family of GTPases and downstream active mechanical processes.

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Cooperative contractility: The role of stress fibres in the regulation of cell-cell junctions

Cited by 14 publications

References 32 publications

Tetrahedral DNA Nanostructure: A Potential Promoter for Cartilage Tissue Regeneration via Regulating Chondrocyte Phenotype and Proliferation

Tetrahedral DNA Nanostructure: A Potential Promoter for Cartilage Tissue Regeneration via Regulating Chondrocyte Phenotype and Proliferation

The role of adhesion junctions in the biomechanical behaviour and osteogenic differentiation of 3D mesenchymal stem cell spheroids

Feedback between mechanosensitive signaling and active forces governs endothelial junction integrity

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