期刊
BIOPHYSICAL JOURNAL
卷 97, 期 7, 页码 1873-1882出版社
CELL PRESS
DOI: 10.1016/j.bpj.2009.07.050
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资金
- National Institute of Arthritis and Musculoskeletal and Skin Diseases [R01 AR053286]
- National Institutes of Health [5 T90 DK70121-03, 5 R90 DK71504-03]
- National Science Foundation [HRD-04,50363)]
The cytoskeleton is known to play an important role in the biomechanical nature and structure of cells, but its particular function in compressive characteristics has not yet been fully examined. This study focused on the contribution of the main three cytoskeletal elements to the bulk compressive stiffness (as measured by the compressive modulus), volumetric or apparent compressibility changes (as further indicated by apparent Poisson's ratio), and recovery behavior of individual chondrocytes. Before mechanical testing, cytochalasin D, acrylamide, or colchicine was used to disrupt actin microfilaments, intermediate filaments, or microtubules, respectively. Cells were subjected to a range of compressive strains and allowed to recover to equilibrium. Analysis of the video recording for each mechanical event yielded relevant compressive properties and recovery characteristics related to the specific cytoskeletal disrupting agent and as a function of applied axial strain. Inhibition of actin microfilaments had the greatest effect on bulk compressive stiffness (similar to 50% decrease compared to control). Meanwhile, intermediate filaments and microtubules were each found to play an integral role in either the diminution (compressibility) or retention (incompressibility) of original cell volume during compression. In addition, microtubule disruption had the largest effect on the critical strain threshold in cellular mechanical behavior (33% decrease compared to control), as well as the characteristic time for recovery (similar to 100% increase compared to control). Elucidating the role of the cytoskeleton in the compressive biomechanical behavior of single cells is an important step toward understanding the basis of mechanotransduction and the etiology of cellular disease processes.
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