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Biophysical Journal 93:4453-4461 (2007)
© 2007 The Biophysical Society

Fibroblast Adaptation and Stiffness Matching to Soft Elastic Substrates

Jérôme Solon * {dagger}, Ilya Levental * {ddagger}, Kheya Sengupta * ¶, Penelope C. Georges * {ddagger} and Paul A. Janmey * §

* Institute for Medicine and Engineering, University of Pennsylvania, Philadelphia, Pennsylvania 19104; {dagger} European Molecular Biology Laboratory, 69117, Heidelberg, Germany; {ddagger} Department of Bioengineering, and § Departments of Physiology and Physics, University of Pennsylvania, Philadelphia, Pennsylvania 19104; and CRMC-N UPR CNRS 7251, Luminy, Marseille, France

Correspondence: Address reprint requests to Dr. Paul Janmey, 1010 Vagelos Labs, 3340 Smith Walk, Philadelphia, PA 19104. Tel.: 215-573-7380; Fax: 215-573-6815; E-mail: janmey{at}mail.med.upenn.edu.

Many cell types alter their morphology and gene expression profile when grown on chemically equivalent surfaces with different rigidities. One expectation of this change in morphology and composition is that the cell's internal stiffness, governed by cytoskeletal assembly and production of internal stresses, will change as a function of substrate stiffness. Atomic force microscopy was used to measure the stiffness of fibroblasts grown on fibronectin-coated polyacrylamide gels of shear moduli varying between 500 and 40,000 Pa. Indentation measurements show that the cells' elastic moduli were equal to, or slightly lower than, those of their substrates for a range of soft gels and reached a saturating value at a substrate rigidity of 20 kPa. The amount of cross-linked F-actin sedimenting at low centrifugal force also increased with substrate stiffness. Together with enhanced actin polymerization and cross-linking, active contraction of the cytoskeleton can also modulate stiffness by exploiting the nonlinear elasticity of semiflexible biopolymer networks. These results suggest that within a range of stiffness spanning that of soft tissues, fibroblasts tune their internal stiffness to match that of their substrate, and modulation of cellular stiffness by the rigidity of the environment may be a mechanism used to direct cell migration and wound repair.




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