Shelly Peyton

Assistant Professor of Chemical Engineering, University of Massachusetts

S. Peyton Lab Website

Ph.D.: University of California, Irvine
Postdoctoral Training: Massachusetts Institute of Technology

Cancer Metastasis, Cell Biomechanics and Bioengineering

The mission of the Peyton lab is to learn how a variety of different cell types are able to process information from biochemical and biophysical cues from the extracellular matrix (ECM), and make decisions about migration and phenotype. To do this, our lab uses both 2D and 3D biomaterial model systems, which can be engineered from the ground-up to instruct cells via both biochemical and biophysical signaling pathways. We focus on applications toward: cardiovascular disease, where tissue homeostasis is normally maintained in a mechanically dynamic ECM; stem-cell therapeutics, where rational scaffold design may be the key to directing appropriate progenitor cell migration and differentiation for tissue regeneration; and cancer, where disruptions in the local ECM microenvironment may cause drastic changes in individual cell motility and phenotype.

Representative recent publications:

S.R. Peyton, Z.I. Kalcioglu, J.D. Cohen, A.P. Runkle, K.J. Van Vliet, D.A. Lauffenburger, and L.G. Griffith (in press) “Marrow-derived stem cell motility in 3D synthetic scaffold is governed by geometry along with adhesivity and stiffness.” Biotechnology and Bioengineering.

C.M. Williams, G. Mehta, S.R. Peyton, A.S. Zeiger, K.J. VanVliet, and L.G. Griffith (2011) “Micropatterned semi-synthetic hydrogel arrays create a 3D niche for autocrine-induced tissue formation.” Tissue Engineering Part A. doi:10.1089/ten.TEA.2010.0398

P.D. Kim, S.R. Peyton, A.J. VanStrien, and A.J. Putnam (2009) “The influence of ascorbic acid, TGF-b1, and cell-mediated remodeling on the bulk mechanical properties of 3-D PEG-fibrinogen constructs.” Biomaterials.  Aug;30(23-24):3854-64

C.B. Khatiwala, P.D. Kim, S.R. Peyton, and A.J. Putnam (2009) “ECM compliance regulates osteogenesis by influencing MAPK signaling downstream of RhoA and ROCK.” Journal of Bone and Mineral Research.  May;24(5):886-98.

S.R. Peyton, P.D. Kim, C.M. Ghajar, D. Seliktar, and A.J. Putnam (2008) “The effects of matrix stiffness and RhoA on the phenotypic plasticity of smooth muscle cells in a 3-D biosynthetic hydrogel system.” Biomaterials. Jun:29(17):2597-607.

C.B. Khatiwala, S.R. Peyton, and A.J. Putnam. (2007) “The regulation of osteogenesis by ECM rigidity in MC3T3-E1 cells requires MAPK activation.” Journal of Cellular Physiology. 211: 661-672.

S.R. Peyton, C.M. Ghajar, C.B. Khatiwala, and A.J. Putnam. (2007) “The emergence of ECM mechanics and cytoskeletal tension as important regulators of cell function.” Cell Biochemistry and Biophysics. Apr;47(2):300–320.

C.M. Ghajar, V. Suresh, S.R. Peyton, C.B. Raub, F.L. Meyskens Jr., S.C. George, and A.J. Putnam. (2007) “A novel 3-D model to quantify metastatic melanoma invasion.” Molecular Cancer Therapeutics. Feb;6(2):552-561.

S.R. Peyton, C.B. Raub, V.P. Keschrumrus, and A.J. Putnam. (2006) “The use of poly(ethylene glycol) hydrogels to investigate the impact of ECM chemistry and mechanics on smooth muscle cells.”  Biomaterials. Oct;27(28):4881-93.

C. Khatiwala, S.R. Peyton, and A.J. Putnam. (2006) “The effects of the intrinsic mechanical properties of the extracellular matrix on the behavior of pre-osteoblastic MC3T3-E1 cells.”  AJP-Cell Physiology. 290(6):C1640-50.

S.R. Peytonand A.J. Putnam. (2005) “Extracellular matrix rigidity governs smooth muscle cell motility in a biphasic fashion.”  Journal of Cellular Physiology. 204(1):198-209.