Dr Bryant Villeponteau the formulator of Stem Cell 100 and other Life Code nutraceuticals was recently interviewed by Dr Mercola who owns the largest health web site on the internet. Dr. Villeponteau is also the author of Decoding Longevity an new book which will be released during December. He is a leading researcher in novel anti-aging therapies involving stem cells an area in which he has been a pioneer for over three decades.
Stem cell technology could have a dramatic influence on our ability to live longer and replace some of our failing parts, which is the inevitable result of the aging process. With an interest in aging and longevity, Dr. Villeponteau started out by studying developmental biology. If we could understand development, we could understand aging, he says. Later, his interest turned more toward the gene regulation aspects. While working as a professor at the University of Michigan at the Institute of Gerontology, he received, and accepted, a job offer from Geron Corporation a Bay Area startup, in the early 90s.
They were working on telomerase, which I was pretty excited about at the time. I joined them when they first started, he says. We had an all-out engagement there to clone human telomerase. It had been cloned in other animals but not in humans or mammals.
If you were to unravel the tip of the chromosome, a telomere is about 15,000 bases long at the moment of conception in the womb. Immediately after conception, your cells begin to divide, and your telomeres begin to shorten each time the cell divides. Once your telomeres have been reduced to about 5,000 bases, you essentially die of old age.
What you have to know about telomerase is that it’s only on in embryonic cells. In adult cells, it’s totally, for the most part, turned off, with the exception of adult stem cells, Dr. Villeponteau explains. Adult stem cells have some telomerase not full and not like the embryonic stem cells, but they do have some telomerase activity.
Most of the research currently being done, both in academia and industrial labs, revolves around either embryonic stem cells, or a second type called induced pluripotent stem cells (iPS). Dr. Villeponteau, on the other hand, believes adult stem cells are the easiest and most efficient way to achieve results.
That said, adult stem cells do have their drawbacks. While they’re your own cells, which eliminates the problem of immune-related issues, there’s just not enough of them. Especially as you get older, there are fewer and fewer adult stem cells, and they tend to become increasingly dysfunctional too. Yet another hurdle is that they don’t form the tissues that they need to form…
To solve such issues, Dr. Villeponteau has created a company with the technology and expertise to amplify your adult stem cells a million-fold or more, while still maintaining their ability to differentiate all the different cell types, and without causing the cells to age. Again, it is the adult stem cells ability to potentially cure, or at least ameliorate, many of our age-related diseases by regenerating tissue that makes this field so exciting.
Dr Villeponteau believes you can add many years, likely decades, to your life simply by eating right, exercising (which promotes the production of muscle stem cells, by the way) and living an otherwise clean and healthy lifestyle. Extreme life extension, on the other hand, is a different matter.
His book, Decoding Longevity, covers preventive strategies to prolong your life, mainly diet, exercise, and supplements. A portion of the book also covers future developments in the area of more radical life extension, such as stem cell technology.
If you would like to read the entire interview here is a link to the text version:
Transcript of Interview With Dr. Bryant Villeponteau by Dr. Joseph Mercola
Now researchers have found a way not just to stop, but, reverse the aging process. The key is something called a telomere. We all have them. They are the tips or caps of your chromosomes. They are long and stable in young adults, but, as we age they become shorter, damaged and frayed. When they stop working we start aging and experience things like hearing and memory loss.
In a recent study published in the peer reviewed journal Nature scientists took mice that were prematurely aged to the equivalent of 80-year-old humans, added an enzyme and essentially turned their telomeres back on. After the treatment they were the physiological equivalent of young adults. You can see the before and after pictures in the videos above. Brain function improved, their fertility was restored it was a remarkable reversal of the aging process. In the top video the untreated mouse shows bad skin, gray hair and it is balding. The mouse with it’s telomeres switched back on has a dark coat color, the hair is restored and the coat has a nice healthy sheen to it. Even more dramatic is the change in brain size. Before treatment the aged mice had 75% of a normal size brain like a patient with severe Alzheimers. After the telomeres were reactivated the brain returned to normal size. As for humans while it is just one factor scientists say the longer the telomeres the better the chances for a more graceful aging.
The formal study Telomere dysfunction induces metabolic and mitochondrial compromise was published in Nature.
Additional information published by Harvard can be found in the following articles.
Scientists Find Root Molecular Cause of Declining Health in the Old
Decoding Immortality – Smithsonian Channel Video about the Discovery of Telomerase
While scientists are not yet able to accomplish the same results in humans we believe we have developed a nutraceutical to help prolong youth and possibly extend life until age reversal therapy for humans becomes available.
New evidence that adult stem cells are critical to human aging has recently been published on a study done on a super-centenarian woman that lived to be 115 years. At death, her circulating stem cell pool had declined to just two active stem cells from stem cell counts that are typically more than a thousand in younger adults. Super-centenarians have survived all the normal diseases that kill 99.9% of us before 100 years of age, so it has been a mystery as to what actually kills these hardy individuals. This recent data suggest that stem cell decline may be the main contributor to aging. If so, stabilizing stem cells may be the best thing one can do to slow your rate of aging.
There are many theories of aging that have been proposed. For example, damage to cells and tissues from oxidative stress has been one of the most popular fundamental theories of aging for more than half a century. Yet antioxidant substances or genes that code antioxidant enzymes have proven largely ineffective in slowing aging when tested in model animals. Thus, interest by scientists has shifted to other hypotheses that might provide a better explanation for the slow declines in function with age.
Stem cells provide one such promising mechanism of aging. Of course, we all know that babies are young and vigorous, independent of the age of their parents. This is because adults have embryonic stem cells that can generate young new cells needed to form a complete young baby. Indeed, these embryonic stem cells are the product of continuously evolving stem cell populations that go back to the beginning of life on earth over 3.5 billion years ago!
In adults, the mostly immortal embryonic stem cells give rise to mortal adult stem cells in all the tissues of the body. These adult stem cells can regenerate your cells and tissues as they wear out and need replacement. Unfortunate, adult stem cells also age, which leads to fewer cells and/or loss of function in cell replacement. As functional stem cells decline, skin and organs decline with age.
Blood from world’s oldest woman suggests life limit
Time Magazine: Long-Life Secrets From The 115-Year-Old Woman
Abstract
The somatic mutation burden in healthy white blood cells (WBCs) is not well known. Based on deep whole-genome sequencing, we estimate that approximately 450 somatic mutations accumulated in the nonrepetitive genome within the healthy blood compartment of a 115-yr-old woman. The detected mutations appear to have been harmless passenger mutations: They were enriched in noncoding, AT-rich regions that are not evolutionarily conserved, and they were depleted for genomic elements where mutations might have favorable or adverse effects on cellular fitness, such as regions with actively transcribed genes. The distribution of variant allele frequencies of these mutations suggests that the majority of the peripheral white blood cells were offspring of two related hematopoietic stem cell (HSC) clones. Moreover, telomere lengths of the WBCs were significantly shorter than telomere lengths from other tissues. Together, this suggests that the finite lifespan of HSCs, rather than somatic mutation effects, may lead to hematopoietic clonal evolution at extreme ages.
A new study that analyzed more than 400 million people has revealed that genetics has a smaller impact on how long a person will live than scientists had previously thought. Researchers from Calico Life Sciences in collaboration with Ancestry (an online genealogy company), have established that inherited life span is much below what was previously estimated as earlier beliefs did not take into account people’s tendency to select partners who had similar traits to their own.
The goal of the study was to assess the heritability of lifespan…whether a person’s parents who lived long lives could predict whether that person lived a long life. Heritability measures to what extent specific genes can explain differences in a person’s traits. In the case of this study, life span. This is different than non genetic differences such as sociocultural factors, lifestyle and accidents. Previous human life span heritability estimates ranged from about 15 to 30 percent.
The researchers looked at a carefully chosen set of family trees and relevant information from over 400 million people who were surveyed by Ancestry. They began with 54 million subscribers to Ancestry which represented six billion ancestors. They then removed entries that were redundant and people who were still living thereby stitching all remaining pedigrees together.
Ancestry then stripped away any identifiable information from pedigrees leaving just the birth year, death year, birth place and familial connections that are part of the family tree structure. Most of the people were based in the U.S. and of European descent and connected to another by either spouse/spouse or parent/child relationship. The researchers then examined the similarity of life span between relatives so they could estimate heritability from each family tree.
They combined statistical and mathematical modeling to analyze data of relatives who were born during the 19th and early 20th centuries. They observed that first cousins and siblings showed same heritability estimates that were observed in previous studies. They also noted the life spans of spouses were likely to be correlated and were actually more similar than in siblings of opposite gender.
The correlation between spouses could be attributed to a variety of non genetic factors such as living in the same household or shared environment. The results then really started to surprise the researchers when they compared different types of first cousins in laws and siblings in law though there was no blood relatives and typically did not share households.
The researchers were able to focus in on correlations for other even more remote relationships which included uncles in laws and aunts, first cousins that are once removed in law and also a variety of configurations of co siblings in law. The findings which indicated that a person’s siblings, spouse siblings or their spouses siblings spouse had similar life spans, made it obvious that something besides a person’s genes was in place.
If people did not share genetic backgrounds and also did not share households, then the question became what best accounts for the life span similarity between individuals that had these types of relationships. The team went back to the data set and proceeded to perform analyses that would detect assortative mating which means the factors which are important to longevity tend to be very similar between mates. People tend to choose partners that have traits similar to their own and in this case how long they live.
Because people marry obviously before one is deceased, then assortative mating must be based on other characteristics. The mate choice could be sociocultural or genetic or both. In regards to non-genetic characteristics, wealthy people tend to marry other wealthy people for example. Or related to genetics, tall people might prefer to marry another tall person and height is somehow correlated to how long a person will live which would also inflate estimates of heritability life span.
The new analysis found that by correcting for the effects of assortative mating, life span heritability is likely no more than seven percent and perhaps even lower. The findings in this study certainly point to how low heritability of lifespan is. There are many things to learn about the biology of aging from human genes, however the recent findings temper expectations about what types of things can be learned and how easy it will be.
o view the original scientific study click here: Estimates of the Heritability of Human Longevity Are Substantially Inflated due to Assortative Mating
Two separate studies have shown that consuming nuts on a daily basis may provide benefits to controlling weight gain, achieving overall metabolic health, and other cardiovascular benefits. Both studies delved into the influence eating nuts has on feeling full and improving insulin and glucose responses. These are things that can influence body weight.
The first study was conducted at the Nutrition Department at the Harvard T. H. Chan School of Public Health in Boston and involved 3 different groups of adults: 25,394 healthy men through Healthy Professionals Follow-up Study, 53,541 women through Nurses’ Health Study and another 47,255 women in Nurses Health Study II. Each of the participants in each group filled out food frequency questionnaires each year for 4 years.
The study team discovered that by replacing foods with less nutritional value with a one once serving of nuts on a daily basis resulted in a lower risk of obesity and weight gain over the 4 year length of the studies. They also found that substituting just one serving a day of nuts instead of one serving of a red meat, processed meat, desserts, potato chips or french fries, resulted in less weight gain. One serving of nuts is one ounce of whole nuts or two tablespoons of a nut butter. The study team believes their findings can be applied to the general population even though most of the participants were part of a health profession and mostly white.
Many people look at nuts as foods that are high in calories and fat and so do not consider them as a healthy snack item. However, the study shows that they actually are associated with less weight gain issues. When people reach adulthood they will begin gaining weight about one pound per year. Over 20 years that is quite a bit of weight gain. Substituting nuts for less nutritionally healthy foods can help prevent this gradual weight gain and also reduce risks of cardiovascular diseases related to weight gain and obesity.
The second study involved Brazil Nuts and was conducted at San Diego State University in 2017 with a grant provided by the American Heart Association. This study involved 22 healthy adults with two men and 20 women all age 20 or older and with a mean body mass index of 22.3. The participants ate either 20 grains of Brazil nuts which is about five nuts or 36 grams of pretzels in addition to their normal diet. The pretzels and Brazil nuts both had about the same number of calories and sodium content. They did this in two trials with 48 hours between each trial.
The team found that both the pretzels and Brazil nuts created reduced hunger feelings and a sense of fullness, however the Brazil nuts created a much fuller feeling of satiety. At forty minutes after the snacks were consumed, the team found the pretzels created a significant increase in insulin and blood glucose levels while the Brazil nuts did not. Brazil nuts actually stabilized both the insulin and blood glucose levels after they were consumed which could be beneficial for preventing weight gain.
Brazil Nuts are very rich in Selenium which is a mineral that might be associated with the insulin and blood glucose improvements noted in the study. Nuts are packed with fiber, protein, unsaturated fatty acids and a variety of beneficial chemicals. Consuming nuts can help reduce appetite and promote fullness which means people tend to eat less throughout the day. In addition to Brazil nuts, almonds, walnuts, pecans, macadamias and pistachios are other good choices!
A new study conducted by researchers at the University of Sao Paulo in Brazil in partnership with colleagues in the U.S. and Norway and published in Scientific Reports, has shown that lack of muscle stimulus results in a buildup of inadequately processed proteins in muscle cells which in turn leads to muscle wasting and weakness. This typical muscle dysfunction is a condition commonly effecting the elderly, individuals who sit for long periods of time without any exercise and bedridden patients.
Test results from rats with induced sciatic nerve injury which stopped receiving stimuli, showed the protein buildup was caused by impairment of autophagy which is the cellular machinery responsible for identifying then removing damaged toxins and proteins. The analysis of the tests on the rats subjected to a regime of aerobic exercise training which were previous to injury enabled the researchers to demonstrate that physical exercise can keep the autophagic system primed and then facilitate its activity as necessary. This is similar to muscle dysfunction due to the lack of stimulus.
Daily exercise will sensitize the autophagic system which facilitates the elimination of organelles (any of a variety of organized or specialized structures within a living cell) and proteins that are not functional in the muscles. It is important that removal of these dysfunctional components occur. When they accumulate they will become toxic and contribute to muscle cell impairment and death.
A good example of what muscle autophagy is, is by comparing muscles working in a similar manner as a refrigerator which runs on electricity. If the signal ceases due to someone pulling the plug on the frig or in the case of muscles blocks the neurons that innervate the muscles, it won’t take too long for food in a frig to spoil and proteins in muscles to spoil at different rates according to their composition. At this point an early warning mechanism in cells activates the autophagic system which will identify, isolate and then incinerate the defective material which prevents propagation of the damage. If the muscles do not receive the right electric signals for long periods of time, the early warning mechanism will stop working properly and cell collapse will occur. Without autophagy, a cascade effect will occur which leads to cell death.
In the current study, rats were submitted to sciatic nerve ligation surgery which created an effect equal to that of sciatic nerve compression in humans. The pain this injury can cause prevents people from using the leg affected by the injury which will lead to weakened muscles and eventually atrophy of those muscles.
Previous to surgery, the rats were divided into two groups. One group remained sedentary while the other group was given exercise training which consisted of running at 60% maximum aerobic capacity for one hour a day, five days per week. After four weeks of exercise training, surgery was performed. The muscular dysfunction induced by sciatic nerve injury was discovered to be less aggressive in the group which had aerobic exercise than the group of rats that were sedentary. Biochemical and functional parameters in the affected muscles were also evaluated. The aerobic training increased autophagic flux and therefore reduced dysfunctional protein levels in the muscles of the rats. Occurring at the same time was improvement in the muscle tissue’s contractility properties. Exercise is a transient stress which will leave memory in the organism and in this case via the autophagic system. When the organism is subjected to a variety of stress, it is better prepared to respond and combat the effects.
The team performed two other experiments which were designed to more thoroughly investigate the link between autophagy and exercise. One experiment involved mice in which the autophagy related gene ATG7 was silenced in the skeletal system. ATG7 encodes a particular protein responsible for synthesizing a vesicle called the autophagosome which forms around dysfunctional organelles and then transports them to the lysosome where they are broken down and then digested. This particular experiment validated the importance of autophagy in muscle biology. ATG7 will knockout mice that had not been subjected to sciatic nerve litigation although displayed muscular dysfunction.
In the second experiment, muscles from rats with sciatic nerve injury and control rats without injury were treated with chloroquine, a drug which inhibits autophagy by raising the lysosomal pH or alkalinity and therefore prevents the degradation of defective proteins. These tests showed less muscle strength in the control group of rats treated with the drug than in the untreated group. Chloroquine had no effect at all on the muscles of the rats with the sciatic nerve injury showing that the inhibition of autophagy is critical to muscular dysfunction caused by lack of stimulus.
Rather than aiming to find a treatment for people who are unable to exercise adequately, the goal of the studies was to use an experimental model for future research to help understand the cellular processes involved in muscle dysfunction. This will help facilitate the development of interventions capable of minimizing or even reversing an increasingly serious problem with muscle weakness and atrophy caused by lack of movement. By identifying a molecule that will selectively keep the autophagic system alert similar to what happens during physical exercise, treatments may be developed which can be given to people with this type of muscle disorder which includes people who are bedridden for extended periods of time, patients with degenerative muscular diseases and the elderly.
To view the original scientific study click here: Exercise prevents impaired autophagy and proteostasis in a model of neurogenic myopathy.
A collaborative study conducted by researchers at Ben Burion University of the Negev and Nanyang Technological University in Singapore, has shown the relative toxicity of six different FDA approved artificial sweeteners (sucralose, aspartame, saccharine, neotame, advantame and acesulfame potassium k) and also 10 sport supplements that contain these ingredients. Bacteria found in the digestive system became toxic when exposed to high levels of the artificial sweeteners such as just one mg/ml.
The team modified bioluminescent E coli bacteria which will illuminate when toxicants are detected and thus become a sensing model representative of the complex microbial system. This provided evidence that artificial sweeteners consumed regulartly adversely affects the activity of gut microbe which can lead to a variety of health issues.
The gut microbial system plays an important role in human metabolism. The study found that mice treated with one artificial sweetener, neotame, had different patterns than those not treated and several important genes found in the human gut decreased. Also noted were high concentrations of several fatty acids, cholesterol and lipids in the mice treated with this artificial sweetener.
Artificial sweeteners are found in many food products and diet soft drink beverages. People consume these added ingredients without even knowing it. This is especially common with athletes who devote a lot of time to their diet which often includes sport supplements taken to improve their physical performance. Additionally, artificial sweeteners have emerged as environmental pollutants and are found in surface and drinking water and in groundwater aquifers.
The study results may help in understanding the toxicity of these sweeteners and the possible negative affects on the gut microbial community and the environment. The bioluminescent bacteria panel might also be used for finding artificial sweetners that could be in the environment.
To view the original scientific study click here: Measuring Artificial Sweeteners Toxicity Using a Bioluminescent Bacterial Panel.
Researchers at the University of Michigan have answered the question that fitness experts and scientists have wondered about. Does nutrition or exercise have the biggest impact on bone strength?
The tests were conducted on male, 16 week old mice which were assigned to 9 groups that were weight matched. This included a baseline group, an exercise with detraining group and a group that was non-exercised. 0.5% Calcium and 0.5% Phosphorus was fed to the control group and 5% Calcium and 1% Phosphorus was fed to the supplemented diet.
The exercise employed was treadmill running for 30 minutes at 12 metres per minute and this lasted for eight weeks. At the end of the eight week period, the mice that consumed the supplemented diet had more BMC (tibial cortical bone mineral content) and vBMD (bone mineral density) than the mice that were in the controlled diet group.
It was additionally noted that exercise was only able to increase BMC when the supplemented diet was also included. At the end of 16 weeks, both exercise and non-exercise groups of mice that were fed a supplemented diet were able to maintain greater tibial cortical BMC as well as vBMD as compared to the mice in the control group.
After looking at exercise and mineral supplementation in mice, they found some very interesting results. Nutrition played a much bigger role in bone strength and mass than exercise. Additionally, after exercise was stopped the mice continued to retain gains in bone strength if they continued to consume a diet supplemented with minerals.
David Kohn, a professor in the schools of engineering and dentistry, noted that long term mineral supplements will lead not only to increases in strength and bone mass, but also the ability to retain the increases even when training stops. And as people age, it is much easier to maintain diet over exercise.
Another finding was that diet alone will have positive effects on bone even when exercise isn’t happening. This was a big surprise to the team who anticipated exercise with a pretty ordinary diet to prove to have bigger gains in a persons bone strength.
Their data indicates that long term use of a mineral supplemented diet can be beneficial in the prevention of bone loss and strength even if you aren’t exercising. Combining both mineral supplementation and exercise serves to amplify the gains.
Previous studies looked at the effects of dietary calcium. The current study looked at increased calcium along with increased phosphorus and discovered benefits by increasing both. This doesn’t mean people should start running out and buying phosphorus and calcium supplements since their findings don’t directly correlate from mice to humans, but it does give the team a concept to study.
It is well known that peak bone mass occurs in people in the early twenties and then begins to decline. The goal then is to figure out how to maximize bone mass at an early age so when bone mass begins to decline, people are able to start in a better position.
The researchers also performed a variety of mechanical assessments that relate to the bone. The mechanical quality of bone tissue doesn’t always correlate with bone mass. The mice were tested following eight weeks of exercise training and a normal diet or a supplemented diet and then following another eight weeks of no training.
To view the original scientific study click here: Combined mineral-supplemented diet and exercise increases bone mass and strength after eight weeks and maintains increases after eight weeks detraining in adult mice.
Neuroscientists from Western University’s Brain and Mind Institute have released early results from the world’s most intense sleep study which reveals that sleeping an average of 7-8 hours per night have better cognitive performance than people that sleep less than that or more.
The article published in SLEEP, shows results from the study which was started in June 2017 with more than 40,000 people from all over the world included in the scientific investigation that was online. The study involved a very detailed questionnaire including a list of cognitive performance activities. The goal was to find out the sleeping habits of people all around the world. Sleep studies of a smaller degree have been conducted in laboratories, however this study’s goal was to find out what sleep is really like.
The study involved a very diverse group of participants which allowed the researchers to compare sleep deprivation on people of different professions, lifestyles and ages. The extensive questionnaire asked questions about where they lived, education level, medications they took and other information that helped the team consider factors that would contribute to results of the study. The participants also underwent 12 established cognitive tests so that mental ability and amount of sleep could be correlated.
About one half of the participants reported that they slept less than 6.3 hours each night. This is about sixty minutes less than what the study recommends for healthy sleep habits. One very surprising revelant factor was that participants who had slept less than four hours performed like they were nine years older than they were.
An additional interesting discovery was the fact that adults were affected equally. People who got seven to eight hours of sleep per night showed the highest functional cognitive behavior and this was regardless of age. The impairment related to too much or too little sleep was not dependent on age. However, older adults were much more likely to have shorter sleep duration which meant they were much more impacted by sleep deprivation than the other age groups of people.
Less sleep and more sleep both negatively impacted several cognitive functions such as information manipulation for problem solving and recognizing complex patterns. Verbal ability and reasoning were the most impacted by sleep with short term memory ability being barely impacted.
The study confirmed that getting 7 to 8 hours of sleep per night is optimal. Data from a previous study conducted on about one million people showed that both sleep deprivation and too many hours sleeping should be avoided for optimal health of the heart. 7 to 8 hours of sleep is recommended to keep the brain performing at its very best.
The studies findings show how significant real world implications are. Many people including those in positions that require a lot of responsibility may operate on too little sleep which may impair problem solving, reasoning and communication skills on a regular basis. Getting too much sleep on the other hand can be just as damaging.
To view the original scientific study click here: Dissociable effects of self-reported daily sleep duration on high-level cognitive abilities.
Researchers have isolated human skeletal stem cells from adult and fetal bones that become cartilage, bone or stroma cells. This is the first time that skeletal stem cells have been identified in humans. The team was also able to derive the skeletal stem cells from human induced pluripotent stem cells which opens up the possibility of therapeutic applications.
By identifying this human skeletal stem cell and elucidating its lineage map, the researchers believe molecular diagnosis and treatment of skeletal diseases will occur. There is a tremendous burden imposed by neoplastic, post traumatic, post surgical and degenerative skeletal disorders. Skeletal dysfunction can develop into a broad spectrum of health conditions and despite its significant impact on disease and health, treatments aimed at improving skeletal function are currently limited. A major hurdle is that stem cell regulation in the human skeletal system is largely unexplored.
Bones posses skeletal tissues which have exceptionally regenerative potential. Defects of the bone heal readily and some vertebrates can actually regenerate portions of their limbs. However, regenerative capacities of skeletal tissues in other vertebrates are much more restricted. Bones in humans and mice can recover from small to moderate sized defects. However, adult cartilage tissue possess little to no regenerative ability. Both humans and mice exhibit severe age related degeneration of skeletal tissues with aging.
In the recent study, the team addressed the knowledge gap by identifying and characterizing human skeletal stem cells and downstream cartilage and bone progeny in a variety of tissues. These self renewing and multipotent cells were present in both adult and fetal human bone marrow tissues. They could be derived from iPSCs (induced pluripotent stem cells). By identifying the relationships between downstream skeletal progenitors and human skeletal stem cells, the team was able to create a lineage map of stem cell mediated formation of human skeletal tissues.
Additionally, transcriptomic (the study of the complete set of RNA transcripts that are produced by the genome under specific circumstances or in a specific cell) and epigenetic (the study of changes in organisms caused by modification of gene expression) comparisons with mouse skeletal stem cells revealed evolutionary conserved pathways regulating stem cell mediated formation of skeletal tissues. Divergent molecular pathways which may regulate species specific differences in skeletal structure and bone development were also revealed.
Comparing functional and molecular differences in specific types of stem cells between different species of vertebrates may lead to the uncovering of divergent and convergent mechanisms which underlie tissue growth and regeneration. This understanding could be applied towards enhancing health and rejuvenation in humans.
To view the original scientific study click here: Identification of the Human Skeletal Stem Cell
