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Nat Commun: The Southern Medical University team revealed why brain damage would accelerate bone healing instead?

 Last Update: 2021-11-01
 Source: Internet
 Author: User

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The brain governs most of the body's physiological functions, from complex cognition, learning and memory, to the regulation of basal body temperature, heart rate and breathing
.

The brain is recognized as the main regulator of peripheral tissue balance; the central regulation of bone remodeling represents a new and expanding field of research

Traumatic brain injury (TBI) is one of the most serious injuries caused by trauma and one of the leading causes of death and disability
.

In patients with long bone fractures, combined TBI is usually observed in a traumatic environment

Clinical evidence in the past fifty years has shown that the accompanying traumatic brain injury accelerates bone healing

Traumatic brain injury accelerates bone healing in patients and rats
.

Traumatic brain injury accelerates bone healing in patients and rats

After TBI, injured neurons, mainly neurons in the hippocampus, can release small extracellular vesicles (sEVs) rich in osteogenic microRNAs (miRNA) to target osteoblasts in the bone to stimulate bone formation After TBI, injured neurons, mainly neurons in the hippocampus, can release small extracellular vesicles (sEVs) rich in osteogenic microRNAs (miRNA) to target osteoblasts in the bone to stimulate bone formation

Researchers have shown that after TBI , miR-328a-3p and miR-150-5p enriched in sEVs promote osteogenesis by directly targeting FOXO4 or the 3′UTR of CBL, respectively .
In addition, sEVs carrying miR-328a-3p The hydrogel can effectively repair bone defects in rats
.

Importantly, the increased expression of fibrin on the surface of sEVs contributes to the targeting effect of TBI sEVs on bone proliferation factors, which means that the modification of fibrin on the surface of sEVs can be used for bone-targeted drug delivery

, MiR-328a-3p and miR-150-5p enriched in sEVs promote osteogenesis by directly targeting FOXO4 or 3′UTR of CBL, respectively .

Original source:

Wei Xia et al.

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