Theranostics

Removing a gene reduced age-related bone loss in mice

In experiments with 12 mice per group, deleting the gene in bone-building cells reduced bone loss after 12 weeks of chemically induced aging.

Paper by Jinli Li, Liyao Zhang, Yuanyuan Ren, 8 more authorsYuyan Xiong · Ministry of Education of the People's Republic of China
Figure 1. Osteoblast-specific knockdown of ARG2 alleviates age-related osteoporosis.
Open the figure at full size
Figure 1. Osteoblast-specific knockdown of ARG2 alleviates age-related osteoporosis.Osteoblast-specific knockdown of ARG2 alleviates age-related osteoporosis.Li et al.
Experiments in male mice with D-galactose-induced aging, against D-gal-treated wild-type miceMechanisms

Randomized, blinded

Limit: Gene-deletion experiments measured chemically induced bone loss, not bone loss during natural aging

Edited by Boris Djordjevic · AgingResearch.News

Follow

In an experiment in male C57BL/6 mice, researchers deleted ARG2, the gene for the enzyme arginase 2, specifically in osteoblasts, the cells that build bone. Groups contained 12 mice. Mice given D-galactose injections for 12 weeks served as a model of age-related bone loss. The study also examined naturally aged, 20-month-old mice.

Deleting ARG2 reduced bone loss and improved the structure of spongy bone in D-galactose-treated mice. It also reduced osteoblast senescence, a state in which cells stop dividing. In mouse bone-building cells grown in the lab, raising arginase 2 levels impaired mitophagy, the process that removes damaged mitochondria, the cell’s energy-producing structures. It also promoted senescence.

Why it matters

Age-associated osteoporosis involves impaired bone-building activity. The findings suggest that targeting arginase 2 may offer an approach to preventing or treating this condition.

Caveats

These experiments in mice and mouse cells did not establish whether targeting arginase 2 would prevent or treat osteoporosis in people.