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Why grow soft?

Scientists have long been growing cells in natural and synthetic matrix environments to elicit phenotypes that are not expressed on conventionally rigid substrates. Unfortunately, growing cells either on or within soft matrices can be an expensive, labor intensive, and impractical undertaking.

Softwell overcomes these challenges. It enables you to study cell behaviors in soft environments with unprecedented efficiency. Furthermore, it provides control over matrix stiffness, a concept that has led to discoveries across a variety of cell types:
  • Stem cell self-renewal1,2
  • Lineage specification3
  • Cancer cell phenotype4,5,6
Remarkably, cells have the ability to sense and respond to changes in matrix stiffness. You can watch this happen in real time in our award-winning movie, Mechanosensing.

Soft substrates for stem cells

Tuning matrix stiffness offers a powerful approach to controlling stem cell fate. Simply culturing them on the proper stiffness has been shown to:

Promote self-renewal. Muscle stem cells derived from mice self-renew and sustain their ability to regenerate damaged muscle tissue in vivo when cultured on substrates replicating the elastic modulus of muscle (E=12 kPa).1

Maintain pluripotency. On E=0.6 kPa substrates, mouse embryonic stem cells generate homogenous undifferentiated colonies in the absence of exogenous LIF.2

Direct lineage specification. Human adult mesenchymal stem cells are directed towards neurogenic, myogenic, and osteogenic lineages on E=1,11, and 34 kPa substrates, respectively.3

Just like the body’s tissues, Softwell is soft and deformable. These physical cues are entirely missed on a rigid Petri dish.


  1. Gilbert, P.M. et al. Substrate elasticity regulates skeletal muscle stem cell self-renewal in culture. Science 329, 1078-1081 (2010).
  2. Chowdhury, F. et al. Soft substrates promote homogeneous self-renewal of embryonic stem cells via downregulating cell-matrix tractions. PLoS ONE 5, e15655 (2010).
  3. Engler, A.J., Sen, S., Sweeney, H.L. & Discher, D.E. Matrix elasticity directs stem cell lineage specification. Cell 126, 677-689 (2006).
  4. Paszek, M.J. et al. Tensional homeostasis and the malignant phenotype. Cancer Cell 8, 241-254 (2005).
  5. Levental, K.R. et al. Matrix crosslinking forces tumor progression by enhancing integrin signaling. Cell 139, 891-906 (2009).
  6. Tilghman, R.W. et al. Matrix rigidity regulates cancer cell growth and cellular phenotype. PLoS ONE 5, e12905 (2010).
  7. Liu, F. et al. Feedback amplification of fibrosis through matrix stiffening and COX-2 suppression. J. Cell Biol 190, 693-706 (2010).
  8. Wipff, P.-J., Rifkin, D.B., Meister, J.-J. & Hinz, B. Myofibroblast contraction activates latent TGF-beta1 from the extracellular matrix. J. Cell Biol 179, 1311-1323 (2007).
  9. Georges, P.C. et al. Increased stiffness of the rat liver precedes matrix deposition: implications for fibrosis. Am. J. Physiol. Gastrointest. Liver Physiol 293, G1147-1154 (2007).
  10. Li, L. et al. Functional modulation of ES-derived hepatocyte lineage cells via substrate compliance alteration. Ann Biomed Eng 36, 865-876 (2008).
  11. Semler, E.J., Lancin, P.A., Dasgupta, A. & Moghe, P.V. Engineering hepatocellular morphogenesis and function via ligand-presenting hydrogels with graded mechanical compliance. Biotechnol. Bioeng 89, 296-307 (2005).
  12. Friedland, J.C., Lee, M.H. & Boettiger, D. Mechanically Activated Integrin Switch Controls α5β1 Function. Science 323, 642 -644 (2009).
  13. Chan, C.E. & Odde, D.J. Traction dynamics of filopodia on compliant substrates. Science 322, 1687-1691 (2008).
  14. Dupont, S. et al. Role of YAP/TAZ in mechanotransduction. Nature 474, 179-183 (2011).