S
Shelly R. Peyton
Researcher at University of Massachusetts Amherst
Publications - 87
Citations - 4037
Shelly R. Peyton is an academic researcher from University of Massachusetts Amherst. The author has contributed to research in topics: Extracellular matrix & Self-healing hydrogels. The author has an hindex of 25, co-authored 76 publications receiving 3361 citations. Previous affiliations of Shelly R. Peyton include Massachusetts Institute of Technology & University of California, Irvine.
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Journal ArticleDOI
Extracellular matrix rigidity governs smooth muscle cell motility in a biphasic fashion.
TL;DR: The mechanical properties of the underlying ECM regulate Rho‐mediated contractility in SMCs by disrupting a presumptive cell‐ECM force balance, which in turn regulates cytoskeletal assembly and ultimately, cell migration.
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The use of poly(ethylene glycol) hydrogels to investigate the impact of ECM chemistry and mechanics on smooth muscle cells
TL;DR: Combined, these data suggest that the mechanical and chemical properties of PEG hydrogels can be tuned to influence SMC phenotype in both 2-D and 3-D.
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Intrinsic mechanical properties of the extracellular matrix affect the behavior of pre-osteoblastic MC3T3-E1 cells.
TL;DR: The conclusion is drawn that altering ECM mechanical properties may influence a variety of MC3T3-E1 cell functions, and perhaps ultimately, their differentiated phenotype.
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The Effects of Matrix Stiffness and RhoA on the Phenotypic Plasticity of Smooth Muscle Cells in a 3-D Biosynthetic Hydrogel System
TL;DR: The synergistic effects of ECM mechanics and RhoA activity on SMC phenotype in 3-D are distinct from those in 2-D, and highlight the importance of studying the mechanical role of cell-matrix interactions in tunable3-D environments.
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ECM Compliance Regulates Osteogenesis by Influencing MAPK Signaling Downstream of RhoA and ROCK
TL;DR: It is established that one possible mechanism by which ECM rigidity regulates osteogenic differentiation involves MAPK activation downstream of the RhoA‐ROCK signaling pathway.