IL-1β decreases the elastic modulus of human tenocytes

Cellular responses to mechanical stimuli are regulated by interactions with the extracellular matrix, which, in turn, are strongly influenced by the degree of cell stiffness (Young's modulus). It was hypothesized that a more elastic cell could better withstand the rigors of remodeling and mechanical loading. It was further hypothesized that interleukin-1β (IL-1β) would modulate intracellular cytoskeleton polymerization and regulate cell stiffness. The purpose of this study was to investigate the utility of IL-1β to alter the Young's modulus of human tenocytes. Young's modulus is the ratio of the stress to the strain, E = stress/strain = (F/A)/(ΔL/L 0), where L 0 is the equilibrium length, ΔL is the length change under the applied stress, F is the force applied, and A is the area over which the force is applied. Human tenocytes were incubated with 100 pM recombinant human IL-1β for 5 days. The Young's modulus was reduced by 27-63%. Actin filaments were disrupted in >75% of IL-1β-treated cells, resulting in a stellate shape. In contrast, immunostaining of α-tubulin showed increased intensity in IL-1β-treated tenocytes. Human tenocytes in IL-1β-treated bioartificial tendons were more tolerant to mechanical loading than were untreated counterparts. These results indicate that IL-1β reduced the Young's modulus of human tenocytes by disrupting the cytoskeleton and/or downregulating the expression of actin and upregulating the expression of tubulins. The reduction in cell modulus may help cells to survive excessive mechanical loading that may occur in damaged or healing tendons. Copyright © 2006 the American Physiological Society.

Full Text

Duke Authors

Cited Authors

  • Qi, J; Fox, AM; Alexopoulos, LG; Chi, L; Bynum, D; Guilak, F; Banes, AJ

Published Date

  • 2006

Published In

Volume / Issue

  • 101 / 1

Start / End Page

  • 189 - 195

International Standard Serial Number (ISSN)

  • 8750-7587

Digital Object Identifier (DOI)

  • 10.1152/japplphysiol.01128.2005

Citation Source

  • SciVal