Clarification of the function of TIMP3 in fracture healing and development of new fracture healing drug

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Monocytes can give rise to osteoclasts (OCs), and dendritic cells (DCs), but these differentiation mechanism is unclear. We clarified that BMSCs up-modulate M-CSF receptor on monocytes through TIMP-3 elaborated by BMSCs to facilitate osteoclastogenesis and suppress DC differentiation, and that TIMP-3 expression is induced in OCs by themselves during osteoclastogenesis to further block TACE activity and enhance the surface expression of M-CSF receptor. This study demonstrated that the suppression of TACE-mediated shedding of M-CSF receptor by BMSCs may dysregulate monocyte differentiation towards OCs to cause bone resorption and anti-inflammatory response in bone remodeling.