Restoring a protein reduced DNA damage in human disc cells
Experiments that altered gene activity in human spinal disc cells found that restoring the protein also reduced senescence, a state in which cells stop dividing.
In experiments with human nucleus pulposus cells, from the centre of spinal discs, researchers studied ZNF865, a protein that regulates many genes. They used gene-targeting tools to turn the activity of the gene that makes it up or down.
Reducing the protein in cells from people without symptoms induced senescence, a state in which cells stop dividing. Restoring it in cells from degenerative discs reduced senescence and DNA damage. Restoration also increased production of the material surrounding cells. It returned gene activity and chromatin accessibility—how readily the cell’s packaged DNA can be accessed—to a healthy state.
Why it matters
Cell senescence contributes to degenerative disc disease, an aging-related condition in which spinal discs deteriorate. The work points to a potential target for addressing senescence and DNA damage in aging-related diseases.
Caveats
The restoration results came from cell experiments, not a treatment study in people. They do not establish whether targeting this protein would relieve back pain in people.
