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Open AccessJournal ArticleDOI

Fibroblast Adaptation and Stiffness Matching to Soft Elastic Substrates

TLDR
Within a range of stiffness spanning that of soft tissues, fibroblasts tune their internal stiffness to match that of their substrate, and modulation of cellular stiffness by the rigidity of the environment may be a mechanism used to direct cell migration and wound repair.
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This article is published in Biophysical Journal.The article was published on 2007-12-15 and is currently open access. It has received 999 citations till now. The article focuses on the topics: Stiffness.

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Citations
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3D hydrogel-based microwell arrays as a tumor microenvironment model to study breast cancer growth.

TL;DR: The microwell array platform developed and characterized in this study could be useful for generating a tissue-specific TME for in vitro high throughput studies of breast cancer development and progression as well as in drug screening studies for breast cancer treatment.
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Mechanosensitivity of Cancer Cells in Contact with Soft Substrates Using AFM

TL;DR: An atomic force microscope in force modulation mode is used to study how local rheological properties of cancer cells are affected by a change of the environment and introduces a paradigm for a new-to- knowledge-possible extravasation mechanism.
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IQGAP1 is a novel phosphatidylinositol 4,5 bisphosphate effector in regulation of directional cell migration

TL;DR: It is shown that type Iγ phosphatidylinositol 4‐phosphate 5‐kinase (PIPKIγ) interacts with the cytoskeleton regulator, IQGAP1, and modulates IQG AP1 function in migration.
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Nanoscale Architecture of the Cortical Actin Cytoskeleton in Embryonic Stem Cells.

TL;DR: By generating a low-density network that physically excludes myosin II, the interplay between Arp2/3, formin, and CP governs the nanoscale architecture of the actin cortex and prescribes the cytomechanical properties of mESCs.
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Feeling Things Out: Bidirectional Signaling of the Cell-ECM Interface, Implications in the Mechanobiology of Cell Spreading, Migration, Proliferation, and Differentiation.

TL;DR: This review covers the current understandings of the key modes of signaling used by both the cell and ECM to coregulate one another and generates an integrated signaling network encompassing the central components of the focal adhesion, cytoplasm and nucleus that act in concert to promote durotaxis, proliferation, and differentiation in a stiffness‐dependent manner.
References
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Journal ArticleDOI

Matrix elasticity directs stem cell lineage specification.

TL;DR: Naive mesenchymal stem cells are shown here to specify lineage and commit to phenotypes with extreme sensitivity to tissue-level elasticity, consistent with the elasticity-insensitive commitment of differentiated cell types.
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Tissue Cells Feel and Respond to the Stiffness of Their Substrate

TL;DR: An understanding of how tissue cells—including fibroblasts, myocytes, neurons, and other cell types—sense matrix stiffness is just emerging with quantitative studies of cells adhering to gels with which elasticity can be tuned to approximate that of tissues.
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Tensional homeostasis and the malignant phenotype.

TL;DR: It is found that tumors are rigid because they have a stiff stroma and elevated Rho-dependent cytoskeletal tension that drives focal adhesions, disrupts adherens junctions, perturbs tissue polarity, enhances growth, and hinders lumen formation.
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Cell Movement Is Guided by the Rigidity of the Substrate

TL;DR: It is discovered that changes in tissue rigidity and strain could play an important controlling role in a number of normal and pathological processes involving cell locomotion, including morphogenesis, the immune response, and wound healing.
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Cell locomotion and focal adhesions are regulated by substrate flexibility

TL;DR: The ability of cells to survey the mechanical properties of their surrounding environment is demonstrated and the possible involvement of both protein tyrosine phosphorylation and myosin-generated cortical forces in this process is suggested.
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