A team of researchers at the RCSI University of Medicine and Health Sciences demonstrated inhibition of microRNAs accelerates bone repair by enhancing the regenerative capacity of bone-forming cells.
MicroRNAs are non-coding RNA molecules that play an important part in gene regulation. The researchers have shown that the delivery of a microRNA silencer increases at a fracture site increases the cells involved in bone repair, while also reducing inflammation and reducing the risk of other complications. The technique could be used on patients who have fractures that do not repair naturally and could potentially be used in patients with degenerative bone diseases.
The researchers use nanoparticles and a collagen-nanohydroxyapatite-microRNA scaffold developed by scientists at the RCSI Tissue Engineering Research Group (TERG), which is implanted surgically. There was no need to pre-seed the scaffold before implantation. The microRNA silencer promotes a local immune response.
The microRNA silencer inhibits miR-133a and encourages the recruitment of CD206+M2-like macrophages. One week following implantation the researchers recorded an increase in calcium deposits, with a 2-fold increase in bone volume. That increased 10-fold after 4-weeks, compared with a scaffold without the microRNA silencer. “An increase in host CD206+ cells suggests an accelerated pro-remodeling response by M2-like macrophages accompanying bone repair with this treatment,” said the researchers.
The RCSI researchers are now exploring other potential uses for their approach, including the repair of articular joints in the knee and hip. They are also exploring whether the delivery of other types of microRNA could be used in a range of novel therapies, including therapies to inhibit breast cancer cell growth.
You can read more about the study in the paper – Rapid bone repair with the recruitment of CD206+M2-like macrophages using non-viral scaffold-mediated miR-133a inhibition of host cells – which was recently published in the journal Acta Biomaterialia. DOI: 10.1016/j.actbio.2020.03.042