화학공학소재연구정보센터
Biochemical and Biophysical Research Communications, Vol.463, No.4, 667-672, 2015
IL-1 beta irreversibly inhibits tenogenic differentiation and alters metabolism in injured tendon-derived progenitor cells in vitro
Tendon injuries are common, and the damaged tendon often turns into scar tissue and never completely regains the original biomechanical properties. Previous studies have reported that the mRNA levels of inflammatory cytokines such as IL-1 beta are remarkably up-regulated in injured tendons. To examine how IL-1 beta impacts tendon repair process, we isolated the injured tendon-derived progenitor cells (inTPCs) from mouse injured Achilles tendons and studied the effects of IL-1 beta on the inTPCs in vitro. IL-1 beta treatment strongly reduced expression of tendon cell markers such as scleraxis and tenomodulin, and also down-regulated gene expression of collagen 1, collagen 3, biglycan and fibromodulin in inTPCs. Interestingly, IL-1 beta stimulated lactate production with increases in hexokinase II and lactate dehydrogenase expression and a decrease in pyruvate dehydrogenase. Inhibition of lactate production restored IL-1 beta-induced down-regulation of collagen1 and scleraxis expression. Furthermore, IL-1 beta significantly inhibited adipogenic, chondrogenic and osteogenic differentiation of inTPCs. Interestingly, inhibition of tenogenic and adipogenic differentiation was not recovered after removal of IL-1 beta while chondrogenic and osteogenic differentiation abilities were not affected. These findings indicate that IL-1 beta strongly and irreversibly impairs tenogenic potential and alters glucose metabolism in tendon progenitors appearing in injured tendons. Inhibition of IL-1 beta may be beneficial for maintaining function of tendon progenitor cells during the tendon repair process. (C) 2015 Elsevier Inc. All rights reserved.