Science & Technology (Commonwealth Union) – A key step in transferring Longevity Gene from Naked Mole Rats to Mice for Enhanced Health and Lifespan
A remarkable feat has been achieved as researchers at the University of Rochester successfully transferred a gene linked to longevity from naked mole rats to mice. This transformative breakthrough not only bolstered the health of the mice but also extended their lifespan.
Naked mole rats, renowned for their prolonged lifespans and remarkable immunity to age-related ailments, have long held the fascination of the scientific world. By introducing a specific gene responsible for augmenting cellular repair and fortification into mice, the team at Rochester University has opened up new avenues for unraveling the enigmas of aging and potentially elongating human lifespan.
Vera Gorbunova, the Doris Johns Cherry Professor of biology and medicine at Rochester, indicated that their study serves as evidence that distinct mechanisms for longevity found in long-lived mammalian species can be harnessed to enhance the lifespans of other mammals. Gorbunova, alongside Andrei Seluanov, a biology professor, and their colleagues, have documented in a Nature publication that they successfully transplanted a gene accountable for producing high molecular weight hyaluronic acid (HMW-HA) from naked mole rats to mice. This intervention yielded heightened well-being and an approximate 4.4 percent increase in the median lifespan of the mice.
Naked mole rats, rodent-sized creatures, exhibit extraordinary longevity for their size, boasting lifespans of up to 41 years, nearly tenfold that of rodents of comparable dimensions. In contrast to numerous other species, naked mole rats rarely fall victim to diseases such as neurodegeneration, cardiovascular issues, arthritis, and cancer as they age. Gorbunova and Seluanov have dedicated decades to exploring the distinctive mechanisms naked mole rats employ to shield themselves against the ravages of aging and diseases.
Previously, these researchers uncovered that HMW-HA constitutes one of the mechanisms underlying the mole rats’ exceptional cancer resistance. In comparison to mice and humans, naked mole rats possess approximately ten times more HMW-HA within their bodies. Upon removal of HMW-HA from naked mole rat cells, the propensity for tumor formation in these cells increased significantly.
Gorbunova, Seluanov, and their collaborators aimed to investigate if the advantageous impacts of HMW-HA could be replicated in other animal species.
The team employed genetic modification to alter a mouse model, causing it to generate the naked mole rat variant of the hyaluronan synthase 2 gene, the gene accountable for producing the protein responsible for HMW-HA. Although all mammals possess the hyaluronan synthase 2 gene, the naked mole rat version appears to be enhanced, leading to heightened gene expression.
The study revealed that mice harboring the naked mole rat version of the gene exhibited heightened resistance against both spontaneous tumors and chemically induced skin cancer. Additionally, these mice displayed improved overall well-being and an extended lifespan in comparison to regular mice. As the mice carrying the naked mole rat gene variant aged, they experienced reduced inflammation across various body regions—a typical marker of aging—and maintained better gut health.
While further investigation is necessary to pinpoint the exact mechanisms behind the favorable effects of HMW-HA, the researchers speculate that these benefits arise from HMW-HA’s capacity to directly regulate the immune system.
Researchers indicated that the findings pave the way for new possibilities for looking into ways HMW-HA could also be utilized to enhance lifespan and lower inflammation-related conditions in humans.
“It took us 10 years from the discovery of HMW-HA in the naked mole rat to showing that HMW-HA improves health in mice,” explained Gorbunova. “Our next goal is to transfer this benefit to humans.”
Researchers stated that they believed they are able to get this through 2 routes: either with the reduction in speed of degradation of HMW-HA or by improving HMW-HA synthesis.
