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Researchers at the University of Virginia School of Medicine have discovered that as we age, our cells’ nuclear membranes become misshapen, which stops our genes from working properly.

Nuclear membranes become distorted with age

The DNA in all our cells is the same; however, the cells in our body show a great range of variation and function. How can this be when they have the same DNA? It all comes down to gene expression and which genes are turned off and which are turned on. For example, certain genes must be turned on in a cell for it to be a liver cell; those same genes need to be turned off for it to be a brain cell. If the correct genes are not turned off, problems occur.

A new study shows that our DNA’s location inside the nucleus is crucial for this process [1]. Genes that are to be switched off are pressed against the nuclear membrane that surrounds the nucleus. However, as cells age, the nuclear membrane becomes misshapen and its surface becomes irregular, causing these genes to remain switched on.

Looking at the liver

During the study, the research team examined a model of fatty liver disease; they found that the liver becomes studded with fat as we age, and this is due to the nuclear membranes in our cells becoming misshapen. Essentially, liver cells are becoming fat cells due to the misshaping of the nuclear membrane causing incorrect gene expression.

The researchers showed that the nuclear membrane becomes misshapen and wrinkled due to a lack of lamin, a protein that comes in a variety of forms and declines with age. They also have a potential solution to this problem: they suggest that we might use viruses to deliver new lamin to the cells.

The hope is that if fresh lamin is delivered to cells, then the shape of their nuclei might be restored and correct gene expression resumed. This could potentially help cells return to a more youthful level of function.

The research team believes that this discovery may help us to understand the aging processes more fully and could give us solutions to diabetes and other age-related diseases.

Conclusion

Delivering fresh lamin to cells is a challenge; however, scientists already use modified viruses to deliver proteins to target cells. The liver is a relatively easy target due to its central role in filtering the bloodstream of toxins. If normal gene expression could be resumed in liver cells, it has the potential to prevent the liver turning to fat with age, keeping it healthy and functional.

Dr. Irina Bochkis, the lead researcher in the study, also believes that this is a universal mechanism in all cells, so restoring lamin could potentially restore nuclear membrane shape and gene expression in all cell types.

Literature

[1] Whitton, H., Singh, L. N., Patrick, M. A., Price, A. J., Osorio, F. G., López‐Otín, C., & Bochkis, I. M. (2018). Changes at the nuclear lamina alter binding of pioneer factor Foxa2 in aged liver. Aging cell, e12742.

About the author

Steve Hill

As a scientific writer and a devoted advocate of healthy longevity and the technologies to promote them, Steve has provided the community with hundreds of educational articles, interviews, and podcasts, helping the general public to better understand aging and the means to modify its dynamics. His materials can be found at H+ Magazine, Longevity reporter, Psychology Today and Singularity Weblog. He is a co-author of the book “Aging Prevention for All” – a guide for the general public exploring evidence-based means to extend healthy life (in press).
  1. July 7, 2018

    I don’t expect miracles, but are there nutritional or other lifestyle changes that are thought to slow or reverse the depletion of lamin?

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