Study summary · research use only
Damaged brain accelerates bone healing by releasing small extracellular vesicles that target osteoprogenitors
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study in rats found that after traumatic brain injury (TBI), injured hippocampal neurons released small extracellular vesicles (sEVs) enriched in osteogenic microRNAs (miRNA) that targeted osteoprogenitors in bone. The abstract reports that miR-328a-3p and miR-150-5p, enriched in sEVs after TBI, were associated with osteogenesis by targeting the 3'UTR of FOXO4 or CBL, and that a hydrogel carrying miR-328a-3p-containing sEVs repaired bone defects in rats. Increased fibronectin on the sEV surface was linked to targeting of osteoprogenitors, suggesting possible use in bone-targeted drug delivery. The authors describe a link between injured neurons and osteoprogenitors reported in both animal and clinical settings.
Abstract
Clinical evidence has established that concomitant traumatic brain injury (TBI) accelerates bone healing, but the underlying mechanism is unclear. This study shows that after TBI, injured neurons, mainly those in the hippocampus, release osteogenic microRNA (miRNA)-enriched small extracellular vesicles (sEVs), which targeted osteoprogenitors in bone to stimulate bone formation. We show that miR-328a-3p and miR-150-5p, enriched in the sEVs after TBI, promote osteogenesis by directly targeting the 3'UTR of FOXO4 or CBL, respectively, and hydrogel carrying miR-328a-3p-containing sEVs efficiently repaires bone defects in rats. Importantly, increased fibronectin expression on sEVs surface contributes to targeting of osteoprogenitors in bone by TBI sEVs, thereby implying that modification of the sEVs surface fibronectin could be used in bone-targeted drug delivery. Together, our work unveils a role of central regulation in bone formation and a clear link between injured neurons and osteogenitors, both in animals and clinical settings.
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