Mechanical stretch in anterior cruciate ligament derived cells regulates type I collagen and decorin expression through extracellular signal-regulated kinase 1/2 pathway

Anterior cruciate ligament (ACL) is continuously exposed to tensile load, which is generally recognized to be an essential factor in maintaining the physiological homeostasis of the ACL fibers during daily activities. Although this kind of mechanical stimulation is clearly known to play an important role in quickening repair of ACL injury, responses of ACL cells to mechanical stimulation still remain unclear. We have investigated whether extracellular signal-regulated kinase 1/2 (ERK1/2) in human ruptured ACL-derived cells are phosphorylated and involved in type I collagen (Col I) and decorin gene expression by mechanical stimulation. Mechanical stretch stimulates time-dependent phosphorylation of ERK1/2 in human ruptured ACL-derived cells. While Col I gene expression levels were increased in 48-h continuous mechanical stretch, decorin gene expression levels were decreased for 24-h continuous stimulation. Decorin gene expression levels were increased, however, in mechanical stretch+PD98059, which is an inhibitor of ERK pathway, treated cells as compared with control cells at 24 h. Our results show that ERK pathway is stimulated by mechanical stretch, and may be involved in regulation of Col I and decorin gene expression in ACL-derived cells.