Interleukin-1beta increases elasticity of human bioartificial tendons

Stiffness is an important mechanical property of connective tissues, especially for tissues subjected to cyclic strain in vivo, such as tendons. Therefore, modulation of material properties of native or engineered tissues is an important consideration for tissue repair. Interleukin 1-beta (IL-1beta) is a cytokine most often associated in connective tissues with induction of matrix metalloproteinases and matrix destruction. However, IL-1beta may also be involved in constructive remodeling and confer a cell survival value to tenocytes. In this study, we investigated the effects of IL-1beta on the properties of human tenocyte-populated bioartificial tendons (BATs) fabricated in a novel three-dimensional (3D) culture system. IL-1beta treatment reduced the ultimate tensile strength and elastic modulus of BATs and increased the maximum strain. IL-1beta at low doses (1, 10 pM) upregulated elastin expression and at a high dose (100 pM) downregulated type I collagen expression. Matrix metalloproteinases, which are involved in matrix remodeling, were also upregulated by IL-1beta. The increased elasticity prevented BATs from rupture caused by applied strain. The results in this study suggest that IL-1beta may act as a defense/survival factor in response to applied mechanical loading. The balance between cell intrinsic strain and external matrix strain is important for maintaining the integrity of tendons.