Claudin 11 regulates bone homeostasis via bidirectional EphB4-EphrinB2 signaling

Abstract

Bone metabolism: A new connection Claudin 11 (Cldn11), a protein that helps form leak-proof connections between cells, also regulates bone density. Claudins are part of tight junctions, which connect cells that form barriers, such as skin cells. Some claudins have been reported to also affect bone metabolism. Ju-Young Kim and Myeung Su Lee from Wonkwang University in Iksan, South Korea, and colleagues investigated how Cldn11 affects bone metabolism. Bone undergoes constant remodeling, and the balance between new bone formation and old bone breakdown is critical. The team found that in cultured cells increasing Cldn11 increased the numbers of bone-forming cells and decreased the numbers of bone-degrading cells. In mice with experimentally induced bone weakness, injection of Cldn11 increased new bone formation and reduced bone resorption. Cldn11 provides a new target to study and treat diseases that cause bone loss, such as osteoporosis.