Abstract
Fracture repair is a complex yet well orchestrated regenerative process involving numerous signaling and cell types including osteoblasts. Here we showed that NPY, a neurotransmitter with regulatory functions in bone homeostasis, may contribute to the post-fracture bone healing in patients with traumatic brain injury-fracture combined injuries. Our results suggested NPY levels were increased in patients with the combined injuries, accomplished by arising of bone healing markers, such as ALP, OC, PICP and ICTP, than in those with simple fractures, and NPY have direct actions on MSCs to promote their osteogenic differentiation. Our results provided clinical evidences for NPY participating in the bone healing process in a nonhypothalamic manner, most probably by directly promoting osteogenesis of mesenchymal stem cells.
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