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!
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!