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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 what about a treatment that not only keeps your muscles flexible during the normal aging process, but also treats various muscle wasting diseases? Well, this is no longer a common concept. The Stanford University School of Medicine researchers have discovered that stem cells, present in the muscle tissues, can prevent tissue scarring, clinically known as fibrosis.

Thomas Rando, who led the study, said: “Fibrosis occurs in many degenerative diseases as well as in normal aging,” he added, “It negatively affects muscle regeneration by changing the stem cell and inhibiting e stem cell function. more scars develop, muscles become stiff and cannot contract and relax smoothly.”

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

The findings of the research are quite amazing. Not only had they discovered that the stem cells in the muscle have the ability to respond to aging, injury or disease, but also they can prevent fibrosis.

The scientists studied PDGFR alpha (PDGFRa), a protein found on the surface of FAPs. The structure and function of the PDGFRa protein is quite intriguing. It straddles the cell membrane. The outer part of the protein functions as a landing area for all external factors that stimulate the FAP cells to divide. The inner part helps to pass the external signal inside. If the response is somehow too enthusiastic, it can lead to fibrosis. So, a balanced response on the part of the stem cell is necessary for an optimal result.

The study showed that the stem cells embedded in muscles can police themselves to get the optimal response. Rando pointed out: “We found 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. “

The normal version of PDGFRa protein instructs the FAPs to divide and grow, which is ideal when FAPs are trying to repair any tissue damage. However, excessive growth can lead to fibrosis. To prevent it, FAPs build a shortened version of PDGFRa protein that orders the cells to prevent tissue scarring by limiting any further division.

The research team found that the stem cells make a shortened version of the protein, which is not present in the interior part. The shortened version of the protein hides the external growth signals away from the larger version of the protein. The cells develop the ability to make the shortened form of the protein by identifying and implementing a series of nucleotides. The nucleotide code then instructs the cell’s messenger RNA to produce a shorter signal. As a result, the protein is broken down.

The researchers forced the FAPs to build the shortened version of the protein in a mouse model. Following the trial, both young and old mice showed less scarring. The team will soon test this approach for muscle-wasting diseases such as muscular dystrophy in a similar mouse model. We will certainly keep you posted on the findings. Stay informed!

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