Source: University of Virginia
Summary: A new discovery about the effects of aging in our cells could allow doctors to cure or prevent diabetes, fatty liver disease and other metabolic diseases and possibly even turn back the clock on aging itself.
We have the same DNA in every single cell but each cell is different. For example, certain genes need to be on in the liver and they have to be turned off in the brain and vice versa. If they’re not turned off appropriately, then we have problems. There’s no wrinkle cream for nuclear membranes, but there is a tantalizing possibility: we might use viruses to smooth the membranes’ surfaces and restore the cells to functioning as they did in the glow of youth. The new finding from the University of Virginia School of Medicine suggests that fatty liver disease and other unwanted effects of aging may be the result of our cells’ nuclei the compartment containing our DNA getting wrinkly. Those wrinkles appear to prevent our genes from functioning properly. The study findings were published in the journal Aging Cell.
This study shows that the location of our DNA inside the cell’s nucleus is critically important. Genes that are turned off are shoved up against the nuclear membrane, which encases the nucleus. But with age, our nuclear membranes become lumpy and irregular, and that prevents genes from turning off appropriately. Looking at a model of fatty liver disease, the team found that our livers become studded with fat as we age because of the wrinkly nuclear membranes. When your nuclear membrane is no longer functioning properly, it can release the DNA that’s supposed to be turned off. So then your little liver cell becomes a little fat cell. The membrane wrinkling stems from a lack of a substance called lamin, a cellular protein that comes in various forms. By putting the appropriate lamin back, we might smooth out the membrane, like Retinol helps smooth facial wrinkles.
Dr. Irina M. Bochkis suspects the wrinkling of the nuclear membrane is responsible for unwanted effects of aging in other parts of the body as well. “Every time I give this talk to colleagues, they say, ‘Well, do you think this is a universal mechanism?'” she said. “In my opinion, I think it is.”
More information: Holly Whitton et al, “Changes at the nuclear lamina alter binding of pioneer factor Foxa2 in aged liver, Aging Cell (2018). DOI: 10.1111/acel.12742