Anisotropic Strain Effects on Vascular Smooth Muscle Cell Physiology

2007 ◽  
Author(s):  
Vadim Tsvankin ◽  
Dmitry Belchenko ◽  
Devon Scott ◽  
Wei Tan
Keyword(s):  
Critical Role ◽  
Stem Cell Differentiation ◽  
Cell Physiology ◽  
Cell Matrix ◽  
Pathological Conditions ◽  
Wide Range ◽  
A Cell ◽  
Biological Development ◽  
Sense And Respond ◽  
Cell Matrix Adhesion

Biological development is a complex and highly-regulated process, a significant part of which is controlled by mechanostimulus, or the strain imparted on a cell by its environment. Mechanostimulus is important for stem cell differentiation, from cytoskeletal assembly to cell-cell and cell-matrix adhesion [1]. The mechanics of cells and tissues play a critical role in organisms, under both physiological and pathological conditions; abnormal mechanotransduction — the mechanism by which cells sense and respond to strain — has been implicated in a wide range of clinical pathologies [2,3].

scholarly journals Probing mechanical principles of focal contacts in cell–matrix adhesion with a coupled stochastic–elastic modelling framework

2011 ◽  
Vol 8 (62) ◽  
pp. 1217-1232 ◽  
Author(s):  
Huajian Gao ◽  
Jin Qian ◽  
Bin Chen
Keyword(s):  
Numerical Models ◽  
Focal Adhesions ◽  
Point Of View ◽  
Matrix Adhesion ◽  
Modelling Framework ◽  
Cell Matrix ◽  
Focal Contacts ◽  
Wide Range ◽  
Sense And Respond ◽  
Cell Matrix Adhesion

Cell–matrix adhesion depends on the collective behaviours of clusters of receptor–ligand bonds called focal contacts between cell and extracellular matrix. While the behaviour of a single molecular bond is governed by statistical mechanics at the molecular scale, continuum mechanics should be valid at a larger scale. This paper presents an overview of a series of recent theoretical studies aimed at probing the basic mechanical principles of focal contacts in cell–matrix adhesion via stochastic–elastic models in which stochastic descriptions of molecular bonds and elastic descriptions of interfacial traction–separation are unified in a single modelling framework. The intention here is to illustrate these principles using simple analytical and numerical models. The aim of the discussions is to provide possible clues to the following questions: why does the size of focal adhesions (FAs) fall into a narrow range around the micrometre scale? How can cells sense and respond to substrates of varied stiffness via FAs? How do the magnitude and orientation of mechanical forces affect the binding dynamics of FAs? The effects of cluster size, cell–matrix elastic modulus, loading direction and cytoskeletal pretension on the lifetime of FA clusters have been investigated by theoretical arguments as well as Monte Carlo numerical simulations, with results showing that intermediate adhesion size, stiff substrate, cytoskeleton stiffening, low-angle pulling and moderate cytoskeletal pretension are factors that contribute to stable FAs. From a mechanistic point of view, these results provide possible explanations for a wide range of experimental observations and suggest multiple mechanisms by which cells can actively control adhesion and de-adhesion via cytoskeletal contractile machinery in response to mechanical properties of their surroundings.

scholarly journals Adhesive multiplicity in the interaction of embryonic fibroblasts and myoblasts with extracellular matrices.

1984 ◽  
Vol 99 (4) ◽  
pp. 1398-1404 ◽  
Author(s):  
C Decker ◽  
R Greggs ◽  
K Duggan ◽  
J Stubbs ◽  
A Horwitz
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Muscle ◽  
Cardiac Fibroblasts ◽  
Cell Types ◽  
Extracellular Matrices ◽  
Common Denominator ◽  
Cell Matrix ◽  
Skeletal Myoblasts ◽  
A Cell ◽  
Cell Matrix Adhesion

Neff et al. (1982, J. Cell Biol., 95:654-666) have described a monoclonal antibody, CSAT, directed against a cell surface antigen that participates in the adhesion of skeletal muscle to extracellular matrices. We used the same antibody to compare and parse the determinants of adhesion and morphology on myogenic and fibrogenic cells. We report here that the antigen is present on skeletal and cardiac muscle and on tendon, skeletal, dermal, and cardiac fibroblasts; however, its contribution to their morphology and adhesion is different. The antibody produces large alterations in the morphology and adhesion of skeletal myoblasts and tendon fibroblasts; in contrast, its effects on the cardiac fibroblasts are not readily detected. The effects of CSAT on the other cell types, i.e., dermal and skeletal fibroblasts, cardiac muscle, 5-bromodeoxyuridine-treated skeletal muscle, lie between these extremes. The effects of CSAT on the skeletal myoblasts depends on the calcium concentration in the growth medium and on the culture age. We interpret these differential responses to CSAT as revealing differences in the adhesion of the various cells to extracellular matrices. This interpretation is supported by parallel studies using quantitative assays of cell-matrix adhesion. The likely origin of these adhesive differences is the progressive display of different kinds of adhesion-related molecules and their organizational complexes on increasingly adhesive cells. The antigen to which CSAT is directed is present on all of the above cells and thus appears to be a lowest common denominator of their adhesion to extracellular matrices.

scholarly journals Mouse placental scaffolds: a three-dimensional environment model for recellularization

2019 ◽  
Vol 10 ◽  
pp. 204173141986796 ◽  
Author(s):  
Rodrigo SN Barreto ◽  
Patricia Romagnolli ◽  
Paula Fratini ◽  
Andrea Maria Mess ◽  
Maria Angelica Miglino
Keyword(s):  
Three Dimensional ◽  
Cell Nuclei ◽  
Embryonic Fibroblasts ◽  
Cell Matrix ◽  
Environment Model ◽  
Collagen Iii ◽  
Culture Substrate ◽  
A Cell ◽  
The Rich ◽  
Cell Matrix Adhesion

The rich extracellular matrix (ECM) and availability make placenta eligible as alternative biomaterial source. Herein we produced placental mouse scaffolds by decellularization, and structure, composition, and cytocompatibility were evaluated to be considered as a biomaterial. We obtained a cell-free scaffold containing 9.42 ± 5.2 ng dsDNA per mg of ECM, presenting well-preserved structure and composition. Proteoglycans were widespread throughout ECM without cell nuclei and cell remnants. Collagen I, weak in native placenta, clearly appears in the scaffold after recellularization, opposite distribution was observed for collagen III. Fibronectin was well-observed in placental scaffolds whereas laminin and collagen IV were strong expressed. Placental scaffolds recellularization potential was confirmed after mouse embryonic fibroblasts 3D dynamic culture, resulting in massive scaffold repopulation with cell–cell interactions, cell-matrix adhesion, and maintenance of natural morphology. Our small size scaffolds provide a useful tool for tissue engineering to produce grafts and organ fragments, as well as for cellular biology purposes for tridimensional culture substrate.

scholarly journals Plexin-B2 orchestrates collective stem cell dynamics via actomyosin contractility, cytoskeletal tension and adhesion

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Chrystian Junqueira Alves ◽  
Rafael Dariolli ◽  
Jonathan Haydak ◽  
Sangjo Kang ◽  
Theodore Hannah ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Molecular Mechanisms ◽  
Cell Physiology ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Actomyosin Contractility ◽  
Cytoskeletal Tension ◽  
Cell Matrix Adhesion ◽  
Cell Cell

AbstractDuring morphogenesis, molecular mechanisms that orchestrate biomechanical dynamics across cells remain unclear. Here, we show a role of guidance receptor Plexin-B2 in organizing actomyosin network and adhesion complexes during multicellular development of human embryonic stem cells and neuroprogenitor cells. Plexin-B2 manipulations affect actomyosin contractility, leading to changes in cell stiffness and cytoskeletal tension, as well as cell-cell and cell-matrix adhesion. We have delineated the functional domains of Plexin-B2, RAP1/2 effectors, and the signaling association with ERK1/2, calcium activation, and YAP mechanosensor, thus providing a mechanistic link between Plexin-B2-mediated cytoskeletal tension and stem cell physiology. Plexin-B2-deficient stem cells exhibit premature lineage commitment, and a balanced level of Plexin-B2 activity is critical for maintaining cytoarchitectural integrity of the developing neuroepithelium, as modeled in cerebral organoids. Our studies thus establish a significant function of Plexin-B2 in orchestrating cytoskeletal tension and cell-cell/cell-matrix adhesion, therefore solidifying the importance of collective cell mechanics in governing stem cell physiology and tissue morphogenesis.

scholarly journals Inositol pyrophosphates promote tumor growth and metastasis by antagonizing liver kinase B1

2015 ◽  
Vol 112 (6) ◽  
pp. 1773-1778 ◽  
Author(s):  
Feng Rao ◽  
Jing Xu ◽  
Chenglai Fu ◽  
Jiyoung Y. Cha ◽  
Moataz M. Gadalla ◽  
...  
Keyword(s):  
Tumor Metastasis ◽  
Cancer Cell Migration ◽  
Cell Matrix ◽  
Promote Tumor Growth ◽  
Wide Range ◽  
Inositol Pyrophosphates ◽  
Liver Kinase B1 ◽  
Tumor Growth And Metastasis ◽  
Cell Matrix Adhesion ◽  
Major Mediator

The inositol pyrophosphates, molecular messengers containing an energetic pyrophosphate bond, impact a wide range of biologic processes. They are generated primarily by a family of three inositol hexakisphosphate kinases (IP6Ks), the principal product of which is diphosphoinositol pentakisphosphate (IP7). We report that IP6K2, via IP7 synthesis, is a major mediator of cancer cell migration and tumor metastasis in cell culture and in intact mice. IP6K2 acts by enhancing cell-matrix adhesion and decreasing cell–cell adhesion. This action is mediated by IP7-elicited nuclear sequestration and inactivation of the tumor suppressor liver kinase B1 (LKB1). Accordingly, inhibitors of IP6K2 offer promise in cancer therapy.

scholarly journals The cancer chemopreventive agent resveratrol induces tensin, a cell–matrix adhesion protein with signaling and antitumor activities

Oncogene ◽  
2005 ◽  
Vol 24 (20) ◽  
pp. 3274-3284 ◽  
Author(s):  
Christelle M Rodrigue ◽  
Françoise Porteu ◽  
Nicole Navarro ◽  
Erik Bruyneel ◽  
Marc Bracke ◽  
...  
Keyword(s):  
Antitumor Activities ◽  
Adhesion Protein ◽  
Chemopreventive Agent ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
A Cell ◽  
Cell Matrix Adhesion

scholarly journals The Role of Mitochondria in the Mechanisms of Cardiac Ischemia-Reperfusion Injury

Antioxidants ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 454 ◽  
Author(s):  
Kuznetsov ◽  
Javadov ◽  
Margreiter ◽  
Grimm ◽  
Hagenbuchner ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Ischemia Reperfusion Injury ◽  
Mitochondrial Dynamics ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Cell Physiology ◽  
Oxygen Species ◽  
Pathological Conditions

Mitochondria play a critical role in maintaining cellular function by ATP production. They are also a source of reactive oxygen species (ROS) and proapoptotic factors. The role of mitochondria has been established in many aspects of cell physiology/pathophysiology, including cell signaling. Mitochondria may deteriorate under various pathological conditions, including ischemia-reperfusion (IR) injury. Mitochondrial injury can be one of the main causes for cardiac and other tissue injuries by energy stress and overproduction of toxic reactive oxygen species, leading to oxidative stress, elevated calcium and apoptotic and necrotic cell death. However, the interplay among these processes in normal and pathological conditions is still poorly understood. Mitochondria play a critical role in cardiac IR injury, where they are directly involved in several pathophysiological mechanisms. We also discuss the role of mitochondria in the context of mitochondrial dynamics, specializations and heterogeneity. Also, we wanted to stress the existence of morphologically and functionally different mitochondrial subpopulations in the heart that may have different sensitivities to diseases and IR injury. Therefore, various cardioprotective interventions that modulate mitochondrial stability, dynamics and turnover, including various pharmacologic agents, specific mitochondrial antioxidants and uncouplers, and ischemic preconditioning can be considered as the main strategies to protect mitochondrial and cardiovascular function and thus enhance longevity.

scholarly journals Talin-bound NPLY motif recruits integrin-signaling adapters to regulate cell spreading and mechanosensing

2014 ◽  
Vol 205 (2) ◽  
pp. 265-281 ◽  
Author(s):  
Perrine Pinon ◽  
Jenita Pärssinen ◽  
Patricia Vazquez ◽  
Michael Bachmann ◽  
Rolle Rahikainen ◽  
...  
Keyword(s):  
Mutational Analysis ◽  
Cell Spreading ◽  
Immune Defense ◽  
Adapter Protein ◽  
Sequence Motifs ◽  
Cell Matrix ◽  
Pathological Conditions ◽  
Dependent Cell ◽  
Cell Matrix Adhesion ◽  
Adjacent Sequence

Integrin-dependent cell adhesion and spreading are critical for morphogenesis, tissue regeneration, and immune defense but also tumor growth. However, the mechanisms that induce integrin-mediated cell spreading and provide mechanosensing on different extracellular matrix conditions are not fully understood. By expressing β3-GFP-integrins with enhanced talin-binding affinity, we experimentally uncoupled integrin activation, clustering, and substrate binding from its function in cell spreading. Mutational analysis revealed Tyr747, located in the first cytoplasmic NPLY747 motif, to induce spreading and paxillin adapter recruitment to substrate- and talin-bound integrins. In addition, integrin-mediated spreading, but not focal adhesion localization, was affected by mutating adjacent sequence motifs known to be involved in kindlin binding. On soft, spreading-repellent fibronectin substrates, high-affinity talin-binding integrins formed adhesions, but normal spreading was only possible with integrins competent to recruit the signaling adapter protein paxillin. This proposes that integrin-dependent cell–matrix adhesion and cell spreading are independently controlled, offering new therapeutic strategies to modify cell behavior in normal and pathological conditions.

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