Placental growth factor mediates mesenchymal cell development, cartilage turnover, and bone remodeling during fracture repair.

ABSTRACT: Current therapies for delayed- or nonunion bone fractures are still largely ineffective. Previous studies indicated that the VEGF homolog placental growth factor (PlGF) has a more significant role in disease than in health. Therefore we investigated the role of PlGF in a model of semi-stabilized bone fracture healing. Fracture repair in mice lacking PlGF was impaired and characterized by a massive accumulation of cartilage in the callus, reminiscent of delayed- or nonunion fractures. PlGF was required for the early recruitment of inflammatory cells and the vascularization of the fracture wound. Interestingly, however, PlGF also played a role in the subsequent stages of the repair process. Indeed in vivo and in vitro findings indicated that PlGF induced the proliferation and osteogenic diff

SUBMITTER: Maes C 

PROVIDER: S-EPMC1435721 | biostudies-literature | 2006 May

REPOSITORIES: biostudies-literature