What happens when the blood of old mice is transfused into young mice?

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Scientists transfused the blood of old mice into young mice. Photo credit: Buena Vista Images/Getty Images.
  • One of the hallmarks of aging is senescence, a condition in which cells stop growing and dividing.
  • A new study shows that a single blood transfusion from old mice causes tissue aging in young mice.
  • Treatment of aged mice with senolytic agents before transfusion into young mice reduced the level of signs of aging in young mice.
  • Research shows that aging can be caused not only by wear and tear, but also by blood-borne factors.

A recently published article Natural metabolism shows that a single transfusion from old mice to young animals can induce stimulation aging — cellular senescence — in young mice.

Identification of factors in the blood of aging animals that may aid in the development of antiaging drugs

The author of the study is Dr. This was reported by Irina Conboy, a professor at the University of California, Berkeley Medical news today:

“[Our study shows that] cellular aging is neither intrinsic to the cell nor purely chronological—an accumulation of damage; In young animals, it occurs quickly within 2 weeks. senolitics It only partially reduces the negative effect of old blood on young cells and tissues and offers additional treatment options.

Dr. Conboy added that this study provides further evidence for the role of factors in the old blood in preventing aging.

Cells undergo injury or stress when they enter a state in which the cell dies or stops proliferating. This state in which cells stop growing and dividing is called cellular senescence.

In addition to external stimuli such as stress, internal factors such as aging and changes in DNA structure can also cause aging.

As the cells age, they can send signals to the immune system, making it easier for them to function removal by immune cells.

A gradual decline in the immune system’s ability to eliminate these senescent cells occurs with aging, resulting in the accumulation of senescent cells. Accumulation of senescent cells contributes to organ aging and is associated with chronic diseases.

Senescent cells may also secrete molecules that signal that neighboring cells are also undergoing senescence. These molecules, released by senescent cells known as the senescence-associated secretory phenotype (SASP), include pro-inflammatory proteins and other factors. reconstruction neighboring tissue.

However, the effect of these factors, secreted by senescent cells, on the propagation of aging is not well understood.

Evidence from previous studies suggests that molecules or cells present in older animals can induce tissue aging in younger animals.

For example, research shows that surgically grafting a young mouse to an older mouse can rejuvenate the tissue of the older mouse. At the same time, this procedure leads to aging of the tissue of a young animal.

In addition to having a common circulatory system, the organs of surgically joined animals are exposed to the same and similar environment. This makes it difficult to identify the potential source of aging or rejuvenating factors.

Similarly, transfusions of blood from old mice to young mice can cause tissue aging in the young animal. These studies suggest that certain factors present in the blood of older mice may predispose their younger counterparts to aging. However, it is unclear whether these antiaging effects of old blood are related to senescent cells.

In this study, the researchers investigated whether aging could be transferred from old mice to young ones through blood transfusions.

To assess the senescence-inducing ability of aged blood, the authors transfused blood from aged mice (22-24 months) into their young counterparts (3 months). The control group consisted of young rats (3 months old) transfused with blood from other young rats of the same age.

Fourteen days after the transfusion, young mice that received blood from older mice showed increased biomarkers of aging in muscle, kidney, and liver. However, there was no such increase in the levels of signs of aging in the lungs, heart and brain.

Young mice transfused from older mice also showed deficits in muscle strength assessments and lower physical endurance.

Similar to skeletal muscle tissue, young mice that received blood from older mice showed higher levels of biomarkers for tissue damage and poor or suboptimal liver and kidney function.

The researchers also transfused blood from young mice into older mice and found that receiving young blood reduced tissue damage in the liver, kidneys and muscles of the older mice.

Taken together, these results suggest that senescence occurs in young mice after blood transfusions from aged mice. In addition, the senescence that occurred in young animals after receiving blood from old mice was tissue-specific.

The researchers then investigated whether the elimination of senescent cells from senescent mice could prevent the induction of senescence in young mice after blood exchange.

For this experiment, the researchers kept old mice in the same routine senolytic drugs Removes old cells in about 4-6 weeks. As expected, treatment with senolytic drugs reduced the levels of secreted factors associated with aging in the plasma of old mice.

The researchers then infused the young mice with blood from older mice treated with senolytic drugs or vehicle.

Young mice that received blood from aged mice treated with senolytics showed reduced signs of aging in muscle, liver, and kidney compared to young mice that received old blood treated with vehicle.

Treatment with senolytics also attenuated the decline in liver, muscle, and kidney function, and reduced damage to these organs in young mice receiving old blood.

In addition, administration of senolytics to aged mice also reduced the adverse effects of old blood on physical activity and energy balance in young mice.

Young mice that received blood from older mice treated with senolytic drugs also showed lower levels of proteins associated with inflammation, a hallmark of aging.

However, young mice receiving blood from senolytic-treated old mice showed some of the adverse effects associated with transfusion of old blood. For example, administration of senolytics to old mice before transfusion did not prevent adverse effects on kidney function in young mice.

These experiments showed that clearance of senescent cells from aged mice reduced the pro-aging effects of transfusing senescent blood into young mice. In other words, aging is not caused by stress or aging, but can also be caused by factors in the old blood.

Further studies are needed to identify factors such as blood molecules, organelles, or senescent cells responsible for the induction of senescence in young mice.

Senescent cells release a number of signaling molecules into the circulation, and these molecules may be responsible, at least in part, for the induction of senescence. Identifying these factors will help develop therapeutic agents to delay the aging process.

Dr. James Kirkland of the Mayo Clinic Kogod Center on Aging told us:

“[This is an] interesting research supporting the efficacy of senolytics in alleviating age-related dysfunction. It confirms and extends previous findings that transplanting senescent cells into young animals causes dysfunction and that removing those senescent cells from transplanted mice restores function, and that transplanting hearts from old to young mice promotes the spread of aging and dysfunction. transplanting hearts from young mice into young mice.

The results of this study raise some interesting questions about aging and potential treatments to slow the aging process.

Dr. Stefan Tullius, director of the Transplantation Surgery Research Laboratory at Brigham and Women’s Hospital”[a]This research raises many open questions in addition to providing us with an improved understanding of aging and the most relevant aspect of its potential for health longevity.

“These open questions mainly concern the clinical relevance of experimental findings: How much blood should be transfused to observe effects? Does a single transfusion make a difference, or should transfusions be significantly greater? How long do the effects last? Are they reversible and ‘one-off’? Is it temporary?”

“The authors report changes that include long-term end-organ damage with scarring in the liver and kidney”. Tullius added.

“Understanding the mechanisms of this process can be very interesting and revealing. Interestingly, functional effects, including impaired physical activity, were observed in the mice. Are they permanent or temporary? Furthermore, if physical capabilities are compromised, can we expect cognitive compromises? “Indeed, the discoveries that have created many interesting discoveries may lead us to develop new authors to understand aging methods for better and healthier aging,” he noted.

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