The role of matrix stiffness in regulating cell behavior

By R. Wells. Hepatology, 2008

1,049 citations recorded by the source corpus.

Subfields: Biomedical Engineering, Cell Biology

View Paper: https://www.semanticscholar.org/paper/c4f776c12608a68624d0ea4b479be4fe790ed3fc

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In Biomedical Engineering

In Cell Biology

Citations in the corpus

Hepatic stellate cells as key target in liver fibrosis (2017, background): “stimuli to activate HSCs at least partially via integrin signaling pathways, forming positive feedback loops [50,51].”
The extracellular matrix modulates the hallmarks of cancer (2014, positive): “Consistently, cells interacting with a stiffer ECM proliferate more in response to growth factors and express genes that positively correlate with a proliferative signature [7,31].”
Feedback amplification of fibrosis through matrix stiffening and COX-2 suppression (2010, background): “…fact that similar stiffness levels and cellular behaviors are observed during fibrogenesis in other soft tissues (Georges et al., 2007; Li et al., 2007; Wells, 2008), we propose that the mechanobiological feedback loop detailed in this study may represent a common feature of progressive fibrosis.”
Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use in investigating mechanisms of hepatotoxicity, cell signaling and ADME (2013, positive): “As expected, isolated hepatocytes de-differentiate when cultured on hard 2D substrates that increase the ECM stiffness to favor a proliferative rather than differentiated cellular phenotype (Wells 2008a, b).”
Extracellular matrix and cell signalling: the dynamic cooperation of integrin, proteoglycan and growth factor receptor. (2011, background): “Matrix stiffness also has effects on cell migration, proliferation and survival (Wells 2008), and focal adhesions can form and grow only if they experience pulling forces through their cytoskeleton.”
Genetic and cell biological analysis of integrin outside-in signaling. (2009, background): “Matrix stiffness also has effects on cell migration, proliferation, and survival (Wells 2008).”
The myofibroblast: paradigm for a mechanically active cell. (2010, background): “What starts the mechanical feedback loop with the ECM—are fibroblast first becoming contractile to stiffen the ECM or is ECM stiffening preceding the fibrotic process, as recently suggested (Wells, 2008)? Considering the heterogeneity of their precursors, are all myofibroblasts equally responsive to”
Evolving challenges in hepatic fibrosis (2010, result): “Extracellular matrix stiffness drives fibrogenesis New diagnostic modalities that correlate the stiffness of the liver with the fibrosis stage (for example, transient elastography [see below]) have found a molecular correlate in studies demonstrating that the physical properties of ECM, in additi”
Recent developments in myofibroblast biology: paradigms for connective tissue remodeling. (2012, background): “Myofibroblasts develop in vitro and in vivo their highly contractile cytoskeletal apparatus only above a certain ECM stiffness threshold.(3,62) Various fibrotic organs and tissues have recently exceeded this threshold at the micromechanical level.”
Myofibroblasts revert to an inactive phenotype during regression of liver fibrosis (2012, background): “Chronic liver injury of any etiology produces fibrosis as a result ofderegulation of the normal healing process with massive accumulation of extracellular matrix (ECM), including type I collagen (ColI) (1).”