Latest news with #CellStemCell
Yahoo
20-07-2025
- Health
- Yahoo
New pocket-size model of ALS 'breathes and flows like human tissue'
When you buy through links on our articles, Future and its syndication partners may earn a commission. Scientists invented a pocket-sized model of the most common form of amyotrophic lateral sclerosis (ALS). The "disease-on-a-chip," made using stem cells, could pave the way for new treatments for the progressive condition, the researchers say. In ALS, the brain and spinal-cord cells that control voluntary muscle movements — known as motor neurons — break down and die. As a result, the brain can no longer send signals to the muscles, leading to symptoms of muscle weakness and paralysis, as well as trouble speaking, swallowing and breathing. In a study published July 3 in the journal Cell Stem Cell, scientists unveiled a new model of sporadic ALS, which accounts for up to 95% of ALS cases and occurs spontaneously without a clear genetic cause or known family history. The platform mimics the early stages of the disease and does so more accurately than previous lab models could. To build the model, researchers collected blood cells from young-onset ALS patients, all under age 45, and healthy male donors, whose cells were used to build a "healthy" chip, for comparison. The blood cells were reprogrammed into induced pluripotent stem cells (iPSCs), which can be turned into any type of cell in the body. The stem cells were then turned into spinal motor neurons, which normally enable movement and degenerate in ALS. A second set of iPSCs was turned into cells similar to the blood-brain barrier (BBB), which helps prevent harmful germs and toxins from entering the brain. The spinal neurons were seeded into one channel within the chip, while the BBB cells were placed in another channel. Separated by a porous membrane, the two chambers were then perfused with nutrient-rich fluid to mimic continuous blood flow. The resulting "spinal-cord chip" maintained both sets of cells for up to about a month and helped the neurons mature beyond what models without flowing fluids allowed. Related: Scientists invent 1st 'vagina-on-a-chip' The basic chip was developed by the biotech company Emulate and then customized for use in the ALS model by researchers at Cedars-Sinai in Los Angeles, California. Earlier models of ALS also used iPSC-derived neurons and structures mimicking those found in the brain, but they lacked dynamic flow, making it hard to capture specific aspects of the disease. "Our previous models were static, like a dish of cells sitting still, and couldn't differentiate between ALS and healthy cells," said study co-author Clive Svendsen, executive director of the Board of Governors Regenerative Medicine Institute at Cedars-Sinai. "We recreated an in vitro [lab dish] environment that breathes and flows like human tissue, which allowed us to detect early differences in ALS neurons." Other experts agree. "Unlike most lab models that lack vascular features and dynamic flow, this chip improves neuron health and maturation," said Dr. Kimberly Idoko, a board-certified neurologist and medical director at Everwell Neuro, who was not involved in the study. "It captures early disease signals in ALS that are often hard to detect," Idoko told Live Science in an email. With their ALS and healthy chips in hand, the researchers analyzed the activity of more than 10,000 genes across all the cells. One of the most striking findings was abnormal glutamate signaling in the neurons within the ALS chip. Glutamate is a major excitatory chemical messenger, meaning it makes neurons more likely to fire and send on a message to additional neurons; its counterpart, GABA, is inhibitory. The team saw increased activity in glutamate receptor genes and decreased activity in GABA receptor genes in the motor neurons, compared to the healthy chip. "We were intrigued to find this increase in glutamate activity," Svendsen said. "Although there was no visible neuron death, we hypothesize this hyperexcitability could trigger degeneration at later stages." RELATED STORIES —Body parts grown in the lab —Scientists developing new 'heart-on-a-chip' —Could mini space-grown organs be our 'cancer moonshot'? This finding aligns with long-standing theories about ALS, which suggest that boosted glutamate signalling contributes to nerve damage. It also corresponds with the mechanism of the ALS drug riluzole, which blocks glutamate. The new chip adds to the evidence for this mechanism and could help reveal how it manifests in the earliest stages, before symptoms would be evident in a patient, Svendsen suggested. While Idoko praised the model, she noted it lacks glial cells — additional nervous-system cells involved in ALS — and doesn't capture the late-stage degeneration seen in ALS. "However, a model like this could conceivably be useful for early drug screening, to study how a drug might cross a barrier similar to the blood-brain barrier, in preparation for animal or human studies," she said. The team is now working toward maintaining the cells in the model for up to 100 days. They also would like to incorporate other cell types, like muscle cells, to fully mimic ALS progression. As motor neurons die off in the disease, muscle cells also waste away. "Our goal is now to build models where more neurons die, so we can better map disease pathways and test treatments in a human-like setting," Svendsen said. For now, the chip offers a window into ALS's earliest molecular changes and a tool to figure out how to detect and slow the disease before irreversible damage occurs. Solve the daily Crossword
Bangkok Post
04-07-2025
- Health
- Bangkok Post
Human heart structure beats 21 days in pig embryo
BEIJING — Chinese scientists have, for the first time, cultivated a beating heart structure with human cells in a pig embryo, reporting that the heart continued to beat for 21 days unaided. The study, led by Lai Liangxue's team from the Guangzhou Institutes of Biomedicine and Health under the Chinese Academy of Sciences, was announced at the International Society for Stem Cell Research's annual meeting in Hong Kong on June 12. Previously, the team had cultivated human kidneys in pigs for up to 28 days. According to a report in Nature on June 13, the team reprogrammed human stem cells by introducing genes to prevent cell death and improve their survival in pigs. At the early blastocyst stage - early in pregnancy when a ball of cells forms - they implanted pre-modified human stem cells into pig embryos, which were then transferred to surrogate sows. Researchers observed embryonic hearts growing to a human-equivalent size, comparable to a fingertip, at the same developmental stage - and still beating, according to the Nature report. Using prelabelled luminescent biomarkers, the researchers reported detecting light from human cells coinciding with an embryonic heartbeat. Nature quoted Lai as saying that modified embryos developed typically sized beating hearts, but the report did not say what proportion of the hearts were human cells. The embryos survived only 21 days. Lai suggested at the meeting, "human cells may disrupt pig heart function". In September 2023, Lai's team generated early human kidneys in pig embryos with 70 per cent human cells, in a study featured as a cover story in Cell Stem Cell. Their technology could revolutionise organ transplants. However, clinical applications may take years to develop. At the same conference, a research team led by Shen Xiling from the University of Texas MD Anderson Cancer Centre announced it had integrated human cells into mouse embryo intestines, livers and even brains. Unlike the technical approach used by Lai's team, the Anderson Cancer Centre team first reprogrammed human stem cells and directly cultivated organoids - or miniature versions of organs grown from stem cells - of the intestine, liver and brain in culture dishes. One month post-birth, around 10% of mice had human intestinal cells; incorporation into the liver and brain was lower. Transplants treat organ failure, but accessibility is limited by a shortage of donor organs. Pigs are suitable donors because they have anatomical similarities to humans, but immune responses that cause human rejection prevent their direct use. Growing human organs in pigs offers a potential solution. This research direction is known as human-animal chimeras, referring to the combination of human and animal cells or tissues within a single organism. However, research on human-animal chimeras has sparked ethical controversies. China introduced regulations last year, stating that human cell transplants into non-human animals for research purposes could only be conducted when other methods could not resolve the research issues. At the conference, Stanford University's Hiromitsu Nakauchi urged further analysis to confirm human origin of the cells in the pig embryo experiment, noting that the localisation of fluorescent cells in the heart made integration with pig cells unclear. Hideki Masaki of the Institute of Science Tokyo added: "For transplantable hearts, organs must be exclusively human to prevent immune rejection." On June 16, Nature
Yahoo
16-06-2025
- Health
- Yahoo
This common molecule could reverse muscle ageing and prevent frailty, scientists say
A common molecule found in the body could be targeted to turn aged muscle cells to become young again, helping prevent frailty in older people, a new study suggests. The populations of developed countries are getting older, leading to higher rates of associated frailty and debilitation among their people. Gradual muscle loss in these populations is accelerated by the poor capacity of muscle tissues in older people to repair injury, especially after falls or surgeries. This leads to a condition called sarcopenia, or low muscle mass, in older people, making them prone to even more frailty and movement problems. Previous studies have shown that muscle stem cells play a key role in repairing such tissue damage, but they become dysfunctional with age. Researchers have been trying to understand how aged stem cells differ from young ones and to find ways to reverse these changes. A new study, published in the journal Cell Stem Cell, reveals that aged mice treated with a naturally occurring molecule in the body called Prostaglandin E2 (PGE2) show improved regeneration and strength of aged muscle. Scientists also found that the PGE2 molecule works by counteracting stem cell ageing. In the study, researchers examined the effects of PGE2 and its related molecule EP4 on the body. Previous research has shown that during muscle injury, PGE2 triggers muscle stem cells to regenerate the muscles of young mice. In aged mice, scientists found that the EP4 production in muscle stem cells was either lacking, or reduced by half compared to levels found in young stem cells. 'PGE2 is an alarm clock to wake up the stem cells and repair the damage. Aging essentially reduces the volume of the alarm and the stem cells have also put on ear plugs,' said study author Yu Xin Wang. The new research has found a way to reset the intensity of this cellular alarm clock. When scientists gave a stable form of PGE2 to aged mice after muscle injury and in conjunction with exercise, they found that the treated mice gained more muscle mass and were stronger compared to untreated ones. 'What amazes me most is that a single dose of treatment is sufficient to restore muscle stem cell function, and that the benefit lasts far beyond the duration of the drug,' Dr Wang said. 'In addition to making new muscle, the stem cells stay in the tissue, where they sustain the effect of the PGE2 and instil the muscle with further capacity to regenerate,' he said. The study found that PGE2 treatment can restore stem cell function and reverse many of the age-related changes in mice muscles. 'PGE2 has been implicated in the regenerative process and signalling for the intestine, liver, and several other tissues, potentially opening up an approach that could restore the renewing capacity of other aged tissues,' Dr Wang said. 'We have discovered that the PGE2 induces rejuvenation of aged muscle stem cells, which leads to functional improvements in muscle repair and strength,' scientists concluded.
The Independent
16-06-2025
- Health
- The Independent
This common molecule could reverse muscle ageing and prevent frailty, scientists say
A common molecule found in the body could be targeted to turn aged muscle cells to become young again, helping prevent frailty in older people, a new study suggests. The populations of developed countries are getting older, leading to higher rates of associated frailty and debilitation among their people. Gradual muscle loss in these populations is accelerated by the poor capacity of muscle tissues in older people to repair injury, especially after falls or surgeries. This leads to a condition called sarcopenia, or low muscle mass, in older people, making them prone to even more frailty and movement problems. Previous studies have shown that muscle stem cells play a key role in repairing such tissue damage, but they become dysfunctional with age. Researchers have been trying to understand how aged stem cells differ from young ones and to find ways to reverse these changes. A new study, published in the journal Cell Stem Cell, reveals that aged mice treated with a naturally occurring molecule in the body called Prostaglandin E2 (PGE2) show improved regeneration and strength of aged muscle. Scientists also found that the PGE2 molecule works by counteracting stem cell ageing. In the study, researchers examined the effects of PGE2 and its related molecule EP4 on the body. Previous research has shown that during muscle injury, PGE2 triggers muscle stem cells to regenerate the muscles of young mice. In aged mice, scientists found that the EP4 production in muscle stem cells was either lacking, or reduced by half compared to levels found in young stem cells. 'PGE2 is an alarm clock to wake up the stem cells and repair the damage. Aging essentially reduces the volume of the alarm and the stem cells have also put on ear plugs,' said study author Yu Xin Wang. The new research has found a way to reset the intensity of this cellular alarm clock. When scientists gave a stable form of PGE2 to aged mice after muscle injury and in conjunction with exercise, they found that the treated mice gained more muscle mass and were stronger compared to untreated ones. 'What amazes me most is that a single dose of treatment is sufficient to restore muscle stem cell function, and that the benefit lasts far beyond the duration of the drug,' Dr Wang said. 'In addition to making new muscle, the stem cells stay in the tissue, where they sustain the effect of the PGE2 and instil the muscle with further capacity to regenerate,' he said. The study found that PGE2 treatment can restore stem cell function and reverse many of the age-related changes in mice muscles. 'PGE2 has been implicated in the regenerative process and signalling for the intestine, liver, and several other tissues, potentially opening up an approach that could restore the renewing capacity of other aged tissues,' Dr Wang said. 'We have discovered that the PGE2 induces rejuvenation of aged muscle stem cells, which leads to functional improvements in muscle repair and strength,' scientists concluded.
The Hindu
16-06-2025
- Health
- The Hindu
Common molecule offers clue to making old muscles young again
As we age, it gets harder to recover from a fall, injury or even a tough workout because the body's muscle-repair system starts to falter. Muscle stem cells (MuSCs), the in-house repair crew, stop dividing and rebuilding tissue, losing their ability to respond to damage. A study in Cell Stem Cell on June 12 suggested this decline may be reversible. The key isn't some futuristic therapy but a molecule already used in hospitals today. Researchers found that five daily injections of prostaglandin E2 (PGE2), a compound involved in inflammation and used clinically to induce labour, restored muscle stem cell function in aged mice. After treatment, older mice regained the ability to regenerate damaged muscle: their muscle fibres grew larger, muscle mass increased, and strength improved by about 20% compared to their untreated peers. The findings are important because PGE2 is naturally produced in the body, particularly after injury. It signals MuSCs to start repairs in young muscle, but in older tissue this signal fades, leaving stem cells inactive even when needed. After PGE2 treatment, aged stem cells 'woke up', resumed dividing, participated in tissue repair, and helped restore the animals' muscle strength. Remarkably, these effects lasted at least two weeks beyond the treatment window, suggesting more than just a temporary boost. Even more strikingly, the outcome held true outside the body. When aged stem cells were treated with PGE2 for just 48 hours in the lab and transplanted into injured muscle, they formed new tissue at levels comparable to young stem cells. Imaging showed that these treated cells engrafted robustly, persisted for weeks, and even expanded in response to subsequent injury — evidence that PGE2 acted directly on the cells themselves, not just their environment. To understand how, the team examined molecular changes inside the cells. PGE2 reopened regions of the genome that had become inaccessible with age. It also dialed down a stress-related pathway called AP-1, which becomes overactive in aging MuSCs. The molecule reset the cells' internal programmes, allowing them to act more like their younger selves. The study adds to an ongoing shift in how scientists think about ageing. For years, researchers believed age-related decline in muscle repair was driven mainly by the environment around stem cells, such as inflammation or scar tissue. But this work adds to evidence that stem cells themselves carry reversible, internal changes, opening the door to therapies that rejuvenate cells directly. The relevance goes far beyond the lab. Sarcopenia affects millions and contributes to frailty, slow recovery, and hospital readmissions in older adults. There are no approved therapies that restore MuSC function. The new study suggests a brief intervention could one day support healing in such situations. More research is required before this therapy can be tested in humans. But by showing that stem cell aging isn't irreversible, this study also opens a new frontier. Anirban Mukhopadhyay is a geneticist by training and science communicator from Delhi.
