HomeHEALTHStudy: How blood stem cells maintain their lifelong potential for self-renewal

Study: How blood stem cells maintain their lifelong potential for self-renewal

Study: How blood stem cells maintain their lifelong potential for self-renewal. A team of scientists has found that cells in a so-called “stem cell niche” are responsible for regenerating themselves for life.

Study in mice stem cells have suggested that niche cells produce a substance that stimulates blood cells and thus retains their ability to regenerate themselves. However, in the process of aging, the production of this element ceases and the blood cells begin to age.

A study led by scientists at the German Cancer Research Center (DKFZ) and the Heidelberg Institute for Stem Cell Technology and Experimental Medicine * (HI-STEM) was published in the journal Nature Communications.

Study: How blood stem cells maintain their lifelong potential for self-renewal
Study: How blood stem cells maintain their lifelong potential for self-renewal

Throughout life, blood cells in the bone marrow ensure that our body is adequately supplied with mature blood cells. In the absence of current cell proliferation, blood cells stay in a deep sleep to protect themselves from damage to the genome, which can lead to cancer.

Hemorrhage, infection, and inflammation act like an alarm clock: suddenly, blood cells begin to divide and produce new cells – for example, providing immune cells to fight infections or compensate for the loss of red blood cells or platelets. With each cell division, stem cells are constantly regenerated, so that the stem cell pool is maintained. This is what scientists call renewal.

“Sleep is essential for this unique stem cell ability,” explains Andreas Trumpp, a stem cell specialist at DKFZ and HI-STEM.

“Unlimited regenerative energy is thought to be a key property of abnormal stem cells, which play a key role in the repair and repair of tissues and organs. However, cancer cells also have this ability. said Trumpp.

A team of investigators led by Andreas Trumpp is now looking to determine which molecular signals control the ability to regenerate themselves. In their current analysis, they found in mice that sleeping blood cells carry large amounts of the protein neogenin-1 (Neo-1) in their face.

In contrast, some blood cells do not produce this receptor. Further research revealed that Neo-1 became a key molecule for regeneration: when researchers implanted a receptor in mice, stem cells were not depleted, thus losing their ability to regenerate, and the animal’s hematopoietic system was prematurely terminated.

Neo-1 is a receptor that enables the stem cell to receive external signals. But where do these vital signs come from, so important in their ability to regenerate themselves ,? Investigators have identified the netin-1 signal molecule as its binding partner and the Neo-1 receptor activator. Netrin-1 is produced by endothelial cells that line fine blood vessels in the bone marrow.

“We extracted netrin-1 from the stem cell niche of the bone marrow. Blood cells then lose their ability to regenerate themselves. Conversely, when netrin-1 production is increased by experimentation, they fall asleep deeper,” said Simon Renders, first study author.

Scientists refer to structures close to stem cells as a stem cell niche. A niche can have both cellular and non-cellular components and has a major impact on the functions and duration of blood cells. Cells carrying Netrin-1 blood capillaries are also part of the niche.

“Our results confirm the important role of stem cell niche in stem cell function as well as the ability to regenerate ourselves and our body health,” Trump explained.

Age-related degeneration of the hematopoietic system can also be observed in animals: With age, bone marrow changes its structure, and smaller blood vessels weaken. Using older mice, scientists have been able to show that this is consistent with the loss of netrin-1.

Blood stem cells initially tried to compensate for this deficiency of their vital signal generator by increasing the formation of Neo-1. However, with age, this compensation is no longer sufficient, and the hematopoietic system is increasingly losing its regenerative capacity. The effect of these changes is on the immune system.

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