Many athletes take painkillers regularly after intense workout sessions. The reason being, any muscle injury, inflammation, soreness, stiffness and aches can be handled with these medicines. But a new study suggests that these anti-inflammatory non-steroidal drugs often harm the muscles rather than doing any good. A Stanford Medicine study supports this view and proposes a new study, based on the inflammatory component to treat muscle degeneration with muscle stem cells.

The stem cells in muscles are scattered across the skeletal muscle tissue. They remain inactive until they are divided by stimulation. When our muscles go through an injury or damage, an inflammatory component activates these muscle stem cells, so they start regenerating the tissue.

The team at Stanford suggests that a molecule, Prostaglandin E2 or PGE2, gets released when the muscle sends the inflammatory signal. This component stimulates the repairing process by aiming at the EP4 receptor, located on the surface of muscle stem cells. The muscle stem cells division is caused by the interaction between PGE2 and EP4, which leads to muscle tissue regeneration.

Dr. Helen Blau, the senior author of the study, said, “Traditionally, inflammation has been considered a natural, but sometimes harmful, response to injury. But we wondered whether there might be a component in the pro-inflammatory signaling cascade that also stimulated muscle repair. We found that a single exposure to prostaglandin E2 has a profound effect on the proliferation of muscle stem cells in living animals. We postulated that we could enhance muscle regeneration by simply augmenting this natural physiological process in existing stem cells already located along the muscle fiber.”

They have conducted a study on a mice model and it reveals that the PGE2 is increased by injuries and that in turn increases the expression of the EP4 receptor. This incident leads the team to the idea of treating the mice with PGE2 pulse, so they can stimulate the muscle stem cells to repair the damage.

Dr. Adelaida Palla, the co-first author explained, “When we gave mice a single shot of PGE2 directly to the muscle, it robustly affected muscle regeneration and even increased strength. Conversely, if we inhibited the ability of the muscle stem cells to respond to naturally produced PGE2 by blocking the expression of EP4 or by giving them a single dose of a nonsteroidal anti-inflammatory drug to suppress PGE2 production, the acquisition of strength was impeded.”

The research clearly shows that painkillers can make the situation worse. Additionally, it also suggests that the molecule; PGE2 can be the natural element to enhance muscle regeneration. Dr. Blau is hopeful that future studies will show more encouraging results with PGE2.  “Our goal has always been to find regulators of human muscle stem cells that can be useful in regenerative medicine. It might be possible to repurpose this already FDA-approved drug for use in muscle. This could be a novel way to target existing stem cells in their native environment to help people with muscle injury or trauma, or even to combat natural aging,” added Dr. Blau.

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Aging is a natural process that no one can deny. But how about a treatment that will not only keep your muscles flexible during the normal aging process, but also treat various muscle wasting diseases? Well, this is no more a mere concept. The Stanford University School of Medicine researchers have discovered that stem cells, present in the muscle tissues, can prevent tissue scarring, clinically termed as fibrosis.

Thomas Rando, who lead the study, said, “Fibrosis occurs in many degenerative diseases and also in normal aging,” he added, “It negatively impacts muscle regeneration by altering the stem cell niche and inhibiting the stem cell function. In addition, as more scarring occurs, muscles become stiff and can’t contract and relax smoothly.”

The team tried to understand how normal muscle tissues regenerate under usual circumstances 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, injuries or diseases, 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 any external factors that encourage the FAP cells to divide. The inner portion helps to pass on the external signal inside. If the response is somehow over-enthusiastic, it may lead to fibrosis. So, a balanced response on the stem cell’s part is required for an optimum result.

The study showed that the muscle-embedded stem cells can police themselves to get the optimum response. Rando pointed out, “We’ve 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 if FAPs try to repair any tissue damage. However, excessive growth may lead to fibrosis. In order to avoid it, FAPs build a truncated version of PDGFRa protein that orders the cells to prevent tissue scarring by restricting any further division.

The research team figured out that the stem cells create a shortened version of the protein, which is not there in the interior portion. The shortened version of the protein hides the external growth signals away from the larger version of the protein. The cells grow the ability to create 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 set up a shorter signal. Consequently, the protein gets truncated.

The researchers forced the FAPs to build the shortened version of the protein in a mouse model. Followed by the process, both young and old mice showed less scarring. The team is soon to test this approach for muscle wasting diseases like muscular dystrophy in a similar mouse model. We will certainly keep you updated on the findings. Stay tuned!

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