Is There a “Fountain of Youth” Gene?
A discovery by researchers at the University of Virginia School of Medicine raises the tantalizing prospect that doctors could use a gene called Oct4 to prevent or delay at least some of the effects of aging. Scientific dogma has long insisted that the gene is inactive in adults, but a release from the university reports that the UVA team has found that Oct4 actually plays a vital role in preventing the underlying cause of most heart attacks and strokes. The release quotes researcher Gary K. Owens, PhD, director of UVA’s Robert M. Berne Cardiovascular Research Center as saying, “Finding a way to augment the expression of this gene in adult cells may have profound implications for promoting health and possibly reversing some of the detrimental effects with aging.”
Unexpected Protective Effect
Oct4 plays a key role in the development of all living organisms, yet until now scientists have thought it was permanently inactivated after embryonic development. Some controversial studies have suggested it might have another function later in life, but the UVA researchers are the first to provide conclusive evidence of that: Owens and his colleagues have determined the gene plays a critical protective role during the formation of atherosclerotic plaques inside blood vessels. The rupturing of these plaques is the underlying cause of many heart attacks and strokes.
The researchers found that Oct4 controls the movement of smooth muscle cells into protective fibrous “caps” inside the plaques – caps that make the plaques less likely to rupture. The researchers also have provided evidence that the gene promotes many changes in gene expression that are beneficial in stabilizing the plaques. This is exciting because studies suggest that it may be possible to develop drugs or other therapeutic agents that target the Oct4 pathway as a means to reduce the incidence of heart attacks or stroke. “Our findings have major implications regarding possible novel therapeutic approaches for promoting stabilization of atherosclerotic plaques,” said Olga A. Cherepanova, PhD, a senior research scientist in Owens’ lab.
One surprising finding from UVA’s research: When the researchers blocked the effect of Oct4 in mice, they thought the atherosclerotic plaques might become smaller, because of the reduced number of smooth muscle cells inside. Instead, the plaques grew larger, less stable and more dangerous, stuffed with lipids, dead cells and other damaging components.
Advancing Regenerative Medicine