Find Formula To Stop Againg But Keep It To Themsleves Stem Cells Have a Neat Trick to Prevent Tissue Scarring

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Stem Cells Have a Neat Trick to Prevent Tissue Scarring

Aging is a natural process that no one can deny. But how about treatments that not only keep your muscles flexible during the normal aging process, but also treat various muscle wasting diseases? Well, it’s not the only concept anymore. Researchers at Stanford University School of Medicine have discovered that stem cells in muscle tissue can prevent tissue scarring, medically known as fibrosis.

“Fibrosis occurs in many degenerative diseases and also in normal aging,” said Thomas Rando, who led the study, adding, “It negatively affects muscle regeneration by altering stem cell niches and inhibiting stem cell function. More scarring appears, muscles stiffen and contractures occur.” can’t do and rest comfortably.”

The team tried to understand how normal muscle tissue regenerates under normal conditions and at the same time how they respond to injury. During the research, they focused on fibro-adipogenic progenitors (FAPs), stem cells that reside in muscle and build the desired connective tissue structure to support muscle regeneration.

The results of the research are very surprising. They discovered that stem cells in muscle have the ability to respond to aging, injury or disease, but they can also prevent fibrosis.

The scientists studied PDGFR alpha (PDGFRa), a protein found on the surface of FAPs. The structure and function of the PDGFRα protein is quite intriguing. It sticks to the cell membrane. The outer part of the protein acts as a landing zone for any external factors that encourage FAP cells to divide. The interior helps the outside signal to enter. If the response is somehow over-enthusiastic, it can lead to fibrosis. Therefore, a balanced response on the part of stem cells is essential for optimal results.

Studies have shown that muscle-embedded stem cells can police themselves to achieve an optimal response. Rando pointed out, “We discovered that the cells actively regulate the production of the inhibitory form of the protein, which is very surprising. If they make less, the degree of fibrosis increases; if they make more, it decreases.”

A normal version of the PDGFRα protein directs FAPs to divide and grow, which is ideal when FAPs are trying to repair any tissue damage. However, overgrowth can lead to fibrosis. To avoid this, FAP makes a truncated version of the PDGFRa protein that commands cells to prevent tissue scarring by restricting further division.

The research team discovered that the stem cells create a shortened version of the protein, which is not present in the interior. The shorter version of the protein blocks external growth signals away from the larger version of the protein. Cells increase their ability to create shorter forms of proteins by recognizing and executing sequences of nucleotides. The nucleotide code then instructs the cell’s messenger RNA to set up a short signal. As a result, the protein is cut.

The researchers forced FAP to make a shortened version of the protein in a mouse model. After the procedure, young and old mice showed less scarring. The team is soon to test this approach in a similar mouse model for muscle-wasting diseases such as muscular dystrophy. We will certainly keep you updated on the findings. Stay tuned!

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