NYU Langone researchers identify HOXA10 gene role in bone repair

Researchers at NYU Langone Health have identified the HOXA10 gene as a critical factor in maintaining the lifelong supply of stem cells required for bone healing. The study, published in Science Advances, utilized genetically engineered mice to observe how the disruption of this gene affects skeletal regeneration.

In the study, researchers removed HOXA10 from mice at six days of age and monitored them for 15 months. The findings revealed a 90% loss of expected stem cells and their descendants. Specifically, the share of stem-cell progenitors in fracture calluses was 48% in mice lacking HOXA10 activity, compared to 76% in control groups.

Lead researcher Philipp Leucht, MD, PhD, explained that HOXA10 preserves healing capacity by acting as a brake on premature maturation, preventing stem cells from turning into bone-building osteoblasts before they are needed. The team also conducted lab experiments using human bone biopsy cells, where silencing three related HOX genes resulted in a decrease in stem-cell numbers.

While the research involved isolated cells and did not test treatments on patients, the findings suggest that HOX genes could serve as potential therapeutic targets for enhancing bone regeneration.