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The body clock protein PER1 slows bone breakdown by turning on inflammation-related genes
Updated
Abstract
Conditional knockout of the PER1 gene in mice resulted in decreased bone mass and increased osteoclasts.
- PER1 inhibits the formation of osteoclasts, which are cells that break down bone tissue.
- Depletion of PER1 led to an increase in osteoclasts and a decrease in osteoblasts, the cells responsible for bone formation.
- Sixteen inflammatory genes were found to be downregulated with the loss of PER1, suggesting a role in osteoclast regulation.
- Knockdown of specific inflammatory genes was associated with increased osteoclast formation, similar to the effects seen with PER1 knockout.
- PER1 knockout mice retain normal circadian rhythms, indicating that targeting PER1 may not disrupt these rhythms.
- The findings suggest a potential link between circadian disruption and inflammatory bone diseases.
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