Semaphoring 3A: an association between traumatic brain injury and enhanced osteogenesis

An accelerated speed of fracture-healing in patients with traumatic brain injury (TBI) is often encountered in clinical practice. However the mechanisms responsible for this phenomenon are remain unclear. After TBI, many cytokines have been reported change their expressions, suggest that the phenomenon of accelerated speed of fracture-healing may be associated with these cytokines. Semaphorin 3A is a secreted cytokine regulated by neural injury, and it is known to guide axon/dendrite growth and neuronal migration. Recent studies suggest that Semaphorin 3A is so far the only molecule that can regulate bone resorption and formation synchronously. However, a Semaphoring 3A which could perhaps induce enhanced osteogenesis under TBI condition has not yet been identified. Therefore, we presume that Semaphoring 3A may play a key role in accelerated fracture-healing under TBI condition, and these will make Sema3A as a promising potential therapeutic target for facilitating fracture healing.