BoneKEy Reports | BoneKEy Watch
Blocking micro RNA miR-92a could stimulate angiogenesis and enhance fracture healing
DOI:10.1038/bonekey.2013.192
Murata et al. measured the plasma concentrations of over 130 microRNA (miRNA) molecules in four patients with trochanteric hip fractures, comparing them with the levels seen in four healthy controls.
The levels of the six miRNA molecules found to be significantly altered were measured in a separate group of 26 fracture patients/controls. One, miR-92a, showed a marked change in levels during fracture healing. Levels of miR-92a remained normal within the first 24 h after fracture but then fell significantly. In patients with a trochanteric hip fracture and in those with a lumbar compression fracture, miR-92a levels remained low for 7 to 14 days and recovered to normal levels only after surgery to repair the fracture.
An antisense oligonucleotide that blocks miR-92a was then used to treat mice with a surgically induced fracture. By 14 days after fracture, treated mice developed a callus that was larger than in controls (total volume 84% greater). By 21 days, the fractures in treated mice showed no boundary and extensive remodeling. Endochondral bone formation was enhanced, and treated mice showed more CD31-positive blood vessels compared to controls, suggesting that blocking miR-92a could lead to stimulation of angiogenesis.
Editor’s comment: Having established potential dysregulation of miR-92a in human osteoporotic fracture, inhibition of this miRNA was examined in murine fracture healing. A more rapid transition from cartilage to bone was seen associated, with increased vasculogenesis. This is a novel avenue for addressing dysfunctional fracture repair.
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