Calcified Tissue International

Shared small RNA changes linked to bone aging in mice

Levels of two gene-regulating RNAs fell and one rose in older versus younger mouse bones and bone cells, and irradiated versus non-irradiated bones.

Experiments in mice and mouse osteocytes, against young mice and non-radiated femursInterventions

Limit: RNA levels and predicted pathways do not directly measure microRNAs' effects on skeletal aging

Edited by Boris Djordjevic · AgingResearch.News

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In experiments in mice, researchers compared thighbones and bone-embedded cells called osteocytes from animals aged 5 and 24 months. They also compared radiation-exposed and unexposed thighbones. They measured microRNAs, small RNA molecules that help regulate gene activity.

Two microRNAs fell across all three comparisons; one rose. The rising molecule, miR-183-5p, regulates a cell-signaling pathway associated with bone health. In a separate experiment, mice received an antibody that blocks sclerostin, a protein that inhibits this pathway. They received 100 milligrams per kilogram weekly, with samples analyzed on day 14. In radiation-exposed bones, the antibody lowered miR-133a-3p, a microRNA that inhibits bone metabolism and function. The authors concluded that the findings identified potential gene-regulating pathways involved in skeletal aging.

Why it matters

Cellular senescence, a state in which cells stop dividing, is involved in skeletal aging. The work points to candidate pathways for investigating this process in both normal aging and radiation-related bone deterioration.

Caveats

The RNA measurements and computer-based pathway analyses did not establish that the shared microRNA changes caused skeletal aging. The findings concern mouse bones and cells, not people.