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Experimental and Computational Investigation of the Role of Stress Fiber Contractility in the Resistance of Osteoblasts to Compression

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Abstract

The mechanical behavior of the actin cytoskeleton has previously been investigated using both experimental and computational techniques. However, these investigations have not elucidated the role the cytoskeleton plays in the compression resistance of cells. The present study combines experimental compression techniques with active modeling of the cell’s actin cytoskeleton. A modified atomic force microscope is used to perform whole cell compression of osteoblasts. Compression tests are also performed on cells following the inhibition of the cell actin cytoskeleton using cytochalasin-D. An active bio-chemo-mechanical model is employed to predict the active remodeling of the actin cytoskeleton. The model incorporates the myosin driven contractility of stress fibers via a muscle-like constitutive law. The passive mechanical properties, in parallel with active stress fiber contractility parameters, are determined for osteoblasts. Simulations reveal that the computational framework is capable of predicting changes in cell morphology and increased resistance to cell compression due to the contractility of the actin cytoskeleton. It is demonstrated that osteoblasts are highly contractile and that significant changes to the cell and nucleus geometries occur when stress fiber contractility is removed.

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Acknowledgements

This work was supported by Science Foundation Ireland (Grant No. 08/RFP/ENM1726), the Irish Research Council for Science and Engineering Technology, and the Irish Centre for High End Computing.

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Correspondence to J. P. McGarry.

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P.P. Weafer and W. Ronan are joint first authors.

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Weafer, P.P., Ronan, W., Jarvis, S.P. et al. Experimental and Computational Investigation of the Role of Stress Fiber Contractility in the Resistance of Osteoblasts to Compression. Bull Math Biol 75, 1284–1303 (2013). https://doi.org/10.1007/s11538-013-9812-y

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  • DOI: https://doi.org/10.1007/s11538-013-9812-y

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