Publisher Health

A single protein can reverse the developmental clock on adult brain cells called astrocytes, morphing them into stem-like cells that produce neurons and other cell types, UT Southwestern researchers report in a PNAS study. The findings might someday lead to a way to regenerate brain tissue after disease or injury.
“We’re showing that it may be possible to reprogram the fate of this subset of brain cells, giving them the potential to rebuild the damaged brain,” said study leader and co-corresponding author Chun-Li Zhang, Ph.D., Professor of Molecular Biology and an Investigator in the Peter O’Donnell Jr. Brain Institute.
During development, mammalian stem cells readily proliferate to produce neurons throughout the brain and cells — called glia — that help support them. Glia help maintain optimal brain function by performing essential jobs like cleaning up waste and insulating nerve fibers. However, the mature brain largely loses that stem cell capacity. Only two small regenerative zones, or niches, remain in the adult brain, Dr. Zhang explained, leaving it with extremely limited capacity to heal itself following injury or disease.
Recent research has suggested that glia can be prompted to produce neurons in some models of brain injury or after genetic manipulation. Although these findings are promising, regenerating healthy brain tissue will require production of multiple cell types, rather than only neurons, said Dr. Zhang.
Looking for a way to spur this “multipotent” regeneration, Dr. Zhang and his colleagues used a genetic engineering technique in adult mouse brains to induce astrocytes, a subset of glia, to produce different transcription factors, proteins pivotal for controlling cell identity. These experiments showed that a single transcription factor — a protein known as DLX2 — appeared to reprogram astrocytes into neural stem-like cells capable of producing neurons and multiple subtypes of glial cells.
The researchers confirmed these findings both using a technique called lineage tracing, in which they followed progeny of the altered astrocytes as they multiplied, as well as marker analysis that showed that these new cells had the expected identities of neurons or glia. Working with the team of co-corresponding author Gary Hon, Ph.D., Assistant Professor of Obstetrics and Gynecology and in the Cecil H. and Ida Green Center for Reproductive Biology Sciences and the Lyda Hill Department of Bioinformatics, global gene expression analysis showed that prompting astrocytes to produce DLX2 appeared to reprogram them into stem-like cells with features of both immature brain cells found earlier in development and cells found in the regenerative niches of the adult brain.
Dr. Zhang and his colleagues suggest that DLX2 might someday be used as a tool to treat traumatic brain injuries, strokes, and degenerative conditions such as Huntington’s disease. Researchers in the Zhang lab are planning to study this approach in animal models.
Current UT Southwestern researchers who contributed to this study include Sergio Cananzi, Lei-Lei Wang, and Yuhua Zou. Other participants include co-lead authors Boxun Li, now at Duke University; Yunjia Zhang, now at the Beijing Genomics Institute, China; Chuanhui Han, now at Peking University, China; and Yang-Xin Fu, now at Tsinghua University, China.
This research was supported by funding from The Welch Foundation (I-1724 and I-1926-20170325), the Decherd Foundation, the Texas Alzheimer’s Research and Care Consortium (TARCC2020), the Kent Waldrep Foundation Center for Basic Research on Nerve Growth and Regeneration, the National Institutes of Health (NS099073, NS092616, NS111776, NS117065, NS088095, DP2GM128203, and UM1HG011996), the Cancer Prevention Research Institute of Texas (CPRIT) (RR140023 and RP190451), the Department of Defense (PR172060), the Burroughs Wellcome Fund (1019804), the Harold C. Simmons Comprehensive Cancer Center, and the Green Center for Reproductive Biology.
Dr. Zhang is a W.W. Caruth, Jr. Scholar in Biomedical Research at UT Southwestern. Dr. Hon is a CPRIT Scholar.

Stress seems to have a negative effect on the learning of movements — at least in mice. This is the conclusion of a recent study at the University of Bonn. According to the study, the neurons of rodents lose some of their contacts with other neurons after stress. The animals also developed motor deficits. The results may be useful for earlier diagnosis and improved therapy of stress-related diseases such as depression. They also document that stress leaves traces in the brain — possibly permanent ones. The study appeared in the journal Translational Psychiatry.
Chronically stressed people often show abnormalities in their motor skills, such as poorer fine motor control. However, how these symptoms occur has hardly been studied so far. “We investigated this question in our study,” explains Prof. Dr. Valentin Stein from the Institute of Physiology II at the University of Bonn.
The researchers used mice as experimental animals, some of which they exposed to a stressful situation for a few days. Meanwhile, they used a special microscopy method to take pictures of the rodents’ brains. They focused on parts of the cerebral cortex responsible for motor control and learning new movements.
“With our method, it is possible to observe one and the same neuron at different points in time,” says Dr. Anne-Kathrin Gellner, a physician at the Department of Psychiatry and Psychotherapy at Bonn University Hospital. “We can therefore see whether and how it changes as a result of stress.”
Stressed mice lose synapses
In fact, the researchers came across a conspicuous feature: after the stressful situation, the neurons studied lost some of their synapses — these are the contacts to other nerve cells. During learning processes, new synapses are usually formed or existing ones are strengthened. Instead, the stressed rodents lost up to 15 percent of their contacts.

Scientists develop a method to genetically label neurons with a single gene of interest in mice by combining the anterograde transsynaptic spread of adeno-associated virus serotype 1 (AAV1) with intersectional gene expression. In two distinct circuits: the retina/primary visual cortex to the superior colliculus and the bilateral motor cortex to the dorsal striatum, injections of AAV1 expressing either Cre or Flpo recombinases and the Cre/Flpo double-dependent AAV into two upstream regions and the downstream region, respectively, were used to label postsynaptic neurons receiving inputs from the two upstream regions.
The body functions via an upstream to downstream flow of information mediated by the brain. Input received through upstream areas like the eyes and ears is distributed to its appropriate downstream region by neurons. Following the expression paths of viruses with viral vector infections and observing light-sensitive proteins in a neuronal population with a fluorescence microscope are some ways in which scientists genetically target these neurons to better understand their structure and function in the overall flow of information. “However, these methods alone are limited in their ability to target neurons that receive monosynaptic inputs from two distinct upstream regions, which in turn inhibits our ability to focus on the structure and function of neurons on a finer scale,” states Kenji Mizuseki, Professor of the Department of Physiology, Osaka City University Graduate School of Medicine.
A Communications Biology paper published February 22 details how Professor Mizuseki led a team of researchers to develop a method they call “intersectional, anterograde transsynaptic targeting system,” that genetically labels neurons with a single gene of interest (GOI), in this case a gene that encodes an enhanced yellow fluorescent protein. They demonstrate this labelling method in two different mouse brain circuits: the retina/primary visual cortex to the superior colliculus and the bilateral motor cortex to the dorsal striatum.
Viral vectors are tools commonly used to deliver genetic material into cells, allowing one to track the genetic path a virus takes as it combines with other cells. This got the team thinking. They could inject viruses with genes at different upstream areas of the brain that once combined in specially prepared downstream regions, would alter the genetic environment to produce this enhanced yellow fluorescent protein that they could observe with a fluorescence microscope. “This combination of existent technology — adeno-associated virus serotype 1 (AAV1) and intersectional expression system (INTRSECT),” states first author of the study, Takuma Kitanishi, “brings the best from both worlds for a labelling method that could exhibit synaptic specificity.”
Using mouse models, the team went to work.
They introduced genetically prepared viruses in the upstream -presynaptic- regions of the right eye and left visual cortex (V1), and in the postsynaptic left superior colliculus (sSC), observing many fluorescence-emitting neurons in the left sSC but not in adjacent regions. “We also observed an absence of fluorescence when either of the upstream viruses was omitted,” adds Prof. Mizuseki. To solidify that the team was indeed observing a specific circuit between the retina/V1 and the sSC, they prepared the whole brain by introducing a viral vector that crosses the blood/brain barrier. In addition to fluorescent neurons in the sSC, the team also observed them in the left ventral geniculate nucleus (LGNv). Since this region does not back project to the retina or V1, they hypothesize that the LGNv contains neurons that integrate inputs from the retina and V1. This additional result and subsequent inquiry from testing the robustness of their work is a peak into the potential focus afforded by their new method.
Moving onto the motor cortex (M2), where it is known that the dorsal striatum (DS) receives inputs from M2, the team wanted to find out if DS neurons were receiving inputs from both left and right M2 regions. Applying their method, they saw the fluorescent protein in all types of DS neurons they examined.
“After these experiments,” states Prof. Mizuseki, “it is clear our method provides a powerful means for determining the locations, numbers, and cell types of neurons receiving monosynaptic inputs from the two defined upstream regions.”
In the future, Prof. Mizuseki expressed interest in expanding this new method by replacing the GOI with one that produces a photosensitive protein that they can then use to excite or suppress neuronal activity with light.
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A collaborative study led by the Monash Biomedicine Discovery Institute (BDI) has discovered a new immune checkpoint that may be exploited for cancer therapy.
The study shows that by inhibiting the protein tyrosine phosphatase PTP1B in T cells, the body’s immune response to cancer can be mobilised, helping to repress tumour growth.
T cells are an essential part of the body’s immune system, helping not only to kill invading pathogens, such as viruses but also cancer cells. However, this study has shown that using a new drug candidate, the abundance of PTP1B in T cells that infiltrate tumours is increased, thereby restraining the ability of T cells to attack tumour cells and combat cancer. These findings have identified PTP1B as an intracellular brake, or checkpoint, reminiscent of the cell surface checkpoint PD-1 — the blockade of which has revolutionised cancer therapy.
The findings are published in the journal Cancer Discovery.
Using mice, scientists from Monash BDI, in conjunction with colleagues at the Peter MacCallum Cancer Centre in Melbourne and Cold Spring Harbor Laboratory in New York, found that by inhibiting PTP1B, using an early-stage injectable drug candidate that has previously been shown to be safe and well-tolerated in humans, the cancer-fighting ability of T cells is enhanced, repressing tumour growth.
Remarkably, the authors showed that the inhibition of this intracellular checkpoint, PTP1B, can also enhance the response to a widely used cancer therapy that blocks the PD-1 checkpoint on the surface of T cells.

Global warming is likely to increase the number of people requiring hospitalization due to critically low sodium levels in the blood, a condition known as hyponatremia. A new study from Karolinska Institutet in Sweden projects that a temperature rise of 2 degrees Celsius would increase the burden on hospitals from hyponatremia by almost 14 percent. The findings are published in The Journal of Clinical Endocrinology and Metabolism.
“Our study is the first to provide precise estimates of how temperature influences the risk of hyponatremia, findings that could be used to inform healthcare planning for adapting to climate change,” says Buster Mannheimer, adjunct senior lecturer at the Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet and the study’s first author.
Climate change is expected to trigger a rise in average global temperatures in the coming decades, resulting in a myriad of heat-related consequences for human health. One of those is hyponatremia, which can occur from a variety of diseases such as heart, renal and liver failure as well as from excessive sweating or fluid intake that dilute the sodium concentration in the blood.
Our bodies need sodium to maintain normal blood pressure, support the function of nerves and muscles and regulate the fluid balance in and around our cells. If blood sodium levels drop, it can lead to nausea, dizziness, muscle cramps, seizures and even coma.
It is well known that hyponatremia cases increase in the summer months. Still, data on temperature thresholds above which risks amplify have been lacking, complicating clinical planning and predictions of health burden in future climate scenarios.
Women and elderly at risk
In the current study, the researchers linked data on Sweden’s entire adult population to information on 24-hour mean temperatures over a nine-year period. In that time, more than 11,000 were hospitalized with a principal diagnosis of hyponatremia, most of whom were women with a median age of 76. Average daily temperatures ranged from -10 to 26 degrees Celsius.

A new way to replicate what happens inside the heart after cardiac arrest could open new avenues for the study of heart regeneration whilst reducing the use of live animals in research, according to a study from the University of Surrey and King’s College London.
Researchers have developed a process that involves obtaining and growing thin slices of pig heart tissue which include both the epicardium — the most external layer of the heart that contains cells that can promote its recovery — and underlying heart-muscle.
The team treated the epicardial slices with stimulating compounds, showing that cells become activated in a way that replicates what happens in the heart after a heart attack. The new process was able to reproduce observations typically obtained in live animal models.
Dr Paola Campagnolo, lead author of the study and Senior Lecturer in Molecular Cardiovascular Sciences at the University of Surrey, said:
“This research typifies the One Health, One Medicine ethos at the University of Surrey, as our model could help us understand how to stimulate the repair process after heart attacks without the need to use live animals in the research. We are hopeful our model could lead to better health outcomes for humans and reduce the reliance on animal experiments in cardiovascular science.”
According to the British Heart Foundation, there are around 7.6 million people living with heart or circulatory disease in the UK. This disease causes a quarter of all deaths in the UK.
The ability of the heart to recover after an injury is severely limited by the low number of regenerating cells within its tissue. The current research models and strategies aimed at improving the heart’s repair process are mainly based on surgical procedures performed on laboratory animals.
Dr Davide Maselli, Postdoctoral Research Associate and first author of the paper, said:
“This work provides an innovative tool to study the healing from a heart attack. We believe that our model could be useful to dissect the role of different cells in the reparative process. In our consideration, it is extremely important that every step forward in this field delivers a clinical perspective for the patients while reducing the burden on research animals.”
The research, published in the journal npj Regenerative Medicine, proposes a system to study the regeneration of the heart in a laboratory dish and could therefore lead to a reduction in the number of small animals used in cardiovascular research.
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Berries, veggies, fish, whole grains and rapeseed oil. These are the main ingredients of the Nordic diet concept that, for the past decade, have been recognized as extremely healthy, tasty and sustainable. The diet can prevent obesity and reduce the risk of cardiovascular disease, type 2 diabetes, high blood pressure and high cholesterol.
Until now, Nordic diet research has primarily been linked to the diet’s positive health effect following weight loss. But a new analysis conducted by University of Copenhagen researchers, among others, makes it clear that a Nordic diet has positive health benefits — regardless of whether one loses weight or not.
“It’s surprising because most people believe that positive effects on blood sugar and cholesterol are solely due to weight loss. Here, we have found this not to be the the case. Other mechanisms are also at play,” explains Lars Ove Dragsted, a researcher and head of section at the University of Copenhagen’s Department of Nutrition, Exercise and Sports.
Together with researchers from Finland, Norway, Sweden and Iceland, Dragsted examined blood and urine samples from 200 people over the age of 50, all with elevated BMI and increased risk of diabetes and cardiovascular disease. The participants were divided into two groups — one provided foods according to Nordic dietary recommendations and a control group on their habitual diet. After six months of monitoring, the result was clear.
“The group that had been on the Nordic diet for six months became significantly healthier, with lower cholesterol levels, lower overall levels of both saturated and unsaturated fat in the blood, and better regulation of glucose, compared to the control group. We kept the group on the Nordic diet weight stable, meaning that we asked them to eat more if they lost weight. Even without weight loss, we could see an improvement in their health,” explains Lars Ove Dragsted.
The fat makes us healthy
Instead of weight loss alone, the researchers point to the unique composition of fats in a Nordic diet as a possible explanation for the significant health benefits.

Women who have had one ovary surgically removed (unilateral oophorectomy) are less likely to become pregnant after in vitro fertilisation and give birth to fewer babies than women with both ovaries. That is according to an extensive meta-analysis published in the journal Fertility and Sterility by researchers at Karolinska Institutet in Sweden.
Whether women’s fertility is affected by the removal of one ovary has been subject to inconclusive data. It was previously believed that the remaining ovary could compensate for the loss in women undergoing treatment with IVF and researchers at Karolinska Institutet have now interrogated the question through a meta-analysis.
“Our meta-study shows that a successful IVF outcome was less likely in women that have only one ovary, compared with women with both intact ovaries,” says Kenny Rodriguez-Wallberg, adjunct professor at the Department of Oncology-Pathology, Karolinska Institutet, and consultant at Karolinska University Hospital. “We have been able to show, for the first time, that the surgical removal of an ovary has an adverse effect on fertility.”
When conducting a meta-study, researchers review published studies to compare their results against their own point of inquiry. In this present study, the researchers identified more than 3,000 papers on the subject, of which 18, published between 1984 and 2018, met their criteria and were selected for the final analysis. Taken together, the papers included 1,057 IVF attempts for women with one ovary and 45,813 for women with two. Five of the studies were included in the analyses of live births, 15 in the analysis of pregnancy rate.
In the group of women with one ovary, the chance of giving birth and of becoming pregnant were both around 30 per cent lower than in the group of women with both ovaries.
“We need to realise the consequences on fertility of removing one ovary,” says Kenny Rodriguez-Wallberg. “Sometimes, the operation is necessary, in the event, say, of a malignant tumour, but it’s important to improve the information we give to women about what it can mean for their chances of having future children. Given that the biological reserve of eggs is already limited, we should, in some cases, also offer these women the opportunity to freeze their eggs ahead of an oophorectomy.”
One reason for the previous belief that fertility was unaffected is that most of the studies carried out were too small to provide a significant result.
The researchers now want to examine if the surgical removal of an ovary has any other health effects, such as the impact that the reduced hormone production might have on the development of other diseases.
The study was financed by the Swedish Research Council, the Swedish Cancer Society, the Swedish Childhood Cancer Foundation, the Cancer Research Funds of Radiumhemmet and Region Stockholm.
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One epigenetic factor as well as one organic anion transporter (OAT1), whose function in the nervous system was hitherto unknown, contribute to the development of chronic pain. The underlying molecular mechanism was identified by a team of researchers led by Dr Daniela Mauceri at the Interdisciplinary Center for Neurosciences (IZN) of Heidelberg University. Using mouse models, the researchers demonstrated that the epigenetic factor, known as HDAC4, influences the expression of genes in neuronal cells involved in the processing of pain. The Heidelberg experiments also revealed that the transporter OAT1 regulates pain sensitivity in the spinal cord. The team hopes their findings will pave the way to new approaches for the treatment of chronic pain.
“Normal, acute physiological pain prevents tissue damage and, in the case of injury, resolves with healing. Chronic pathological pain, however, persists after the injury has mended and can manifest even in the absence of a cause,” explains Daniela Mauceri, whose research group works in the Neurobiology department at the IZN. The transition from acute to chronic pain is caused by alterations in gene expression, which regulates how the information contained in a gene is converted to a gene product, such as proteins or RNA molecules. Chronic pain results especially when cells such as the neurons in the dorsal horn are affected. The dorsal horn is the region of the spinal cord which processes sensory information.
The researchers have now identified an epigenetic factor — Histone Deacetylase 4 (HDAC4) — that is a key player in the gene expression of neurons in the dorsal horn. In mouse experiments, they found that long-lasting pain triggered the export, and thus inactivation, of HDAC4 from the nucleus of dorsal horn neurons. If HDAC4 preferentially accumulates in the cytosol, the region outside of the nucleus within each cell, chronic pain-related responses occur. When the researchers prevented HDAC4 from reaching the cytosol, the chronic pain responses in the mice were smaller.
In cooperation with Prof. Dr Rohini Kuner, who leads a working group at the Institute of Pharmacology at the Medical Faculty Heidelberg, Dr Mauceri’s team then explored the question of which genes controlled by HDAC4 are responsible for the transition to chronic pain. They discovered that the central player in this process is Organic Anion Transporter 1 (OAT1), a transporter also expressed in humans. According to Dr Mauceri, its role in the nervous system was unclear until now. “In mouse experiments, we were able to show that, in the spinal cord, OAT1 controls pain sensitivity. If the same can be confirmed in the human context in future studies, this might open up a new therapeutic avenue for the management of chronic pain,” reports the neurobiologist.
To further test this approach, the researchers administered the OAT1 blocker Probenecid to the mice. After this medication was administered, the OAT1 activity decreased, along with the pain-triggered hypersensitivity in the mice. One especially interesting finding was that, in the experiment, Probenecid also provided relief even after chronic pain was already present. The researchers hope their results will open up new treatment approaches for pain if confirmed in future clinical studies. Dr Mauceri: “OAT1 inhibitors like Probenecid, which can be administered directly into the spinal cord using pain pumps, might be interesting to test as a treatment option in chronic pain patients.”
The research work was conducted under the auspices of Heidelberg University’s Collaborative Research Centre 1158, “From nociception to chronic pain: Structure-function properties of neural pathways and their reorganization,” whose spokesperson is Prof. Kuner. The results of the study were published in the journal Nature Communications.
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SARS-CoV-2 viruses can hide from recognition by the immune system. However, the antiviral immune receptor RIG-I can be stimulated, which improves protection against lethal SARS-CoV-2 infections. Researchers led by Prof. Dr. Gunther Hartmann from the Institute of Clinical Chemistry and Clinical Pharmacology at the University Hospital Bonn, in cooperation with other members of the cluster of excellence ImmunoSensation2 at the University of Bonn, have shown this in mice. Also, the incidence of severe disease progression was observed to be significantly reduced. The study was published online in advance in the journal Molecular Therapy — Nucleic Acids and is now available in the final version.
The ongoing SARS-CoV-2 pandemic has caused an imminent urge for both antiviral therapeutical drugs and vaccines. While the development of vaccines was accomplished in a remarkably short timeframe, the identification of direct antiviral treatments has progressed comparatively slowly. In the light of the further risk of pandemics in the future, however, there remains need for direct antiviral drugs and treatments. Moreover, emerging immune-evasive, I.e. camouflaged from the immune system, SARS-CoV-2 variants are of concern. These cause high numbers of infections even in a highly immunized population, underscoring the continuing need for effective antiviral drugs to treat COVID-19.
SARS-CoV-2 belongs to the genus Betacoronavirus. Like other members of this genus, SARS-CoV-2 is equipped with several molecular tools that allow it to evade recognition by the immune system. The virus carries the information to produce a series of proteins, capable of inhibiting antiviral recognition systems of the infected cell. Actually, these systems could identify viral genetic material (here: Ribonucleic acids/RNAs) and sound the alarm. Proteins of SARS-CoV-2 can alter viral ribonucleic acids in a way, that they become indistinguishable from endogenous RNA.
Camouflage protects virus from immune system
For example, viral RNAs are masked by the addition of a methyl group. In this way, the viral RNA escapes early recognition by the central antiviral immune-receptor RIG-I. This receptor normally induces a so called innate immune response in which antiviral active proteins, cell signals and messenger substances — such as type I interferon (IFN) — are generated.
“A robust, early type I IFN production is key to clearing SARS-CoV-2 infection. Its absence is associated with disease progression and the development of severe COVID-19,” Prof. Dr. Eva Bartok from the Institute of Clinical Chemistry and Clinical Pharmacology at the University Hospital Bonn (UKB) explained. The PhD Student and first author Samira Marx added, “The activation of an innate antiviral response, including the release of type I and type III IFNs, is also extremely important for the development of an appropriate antiviral adaptive immune response.” The adaptive immune response occurs only after a few days and involves the activation of further immune cells and ultimately the production of antibodies.
The immune receptor RIG-I has previously been identified as a suitable target for prophylactic triggering of antiviral effects. For example, mouse models have shown that prophylactic stimulation of RIG-I can protect mice from lethal influenza virus infection. “Such RIG-I stimulating RNAs that mimic viral RNA can be chemically synthesized and used as therapeutics to turn the innate immune response against numerous illnesses including cancer and viral infections,” said Prof. Dr. Martin Schlee from the Institute of Clinical Chemistry and Clinical Pharmacology. In the present study, the scientists analyzed the effect of synthetic 5’triphopsphorylated dsRNA (3pRNA) on the course of infection with SARS-CoV-2 in a mouse model.
Mouse model to resemble human COVID-19 infection
As mice are generally not susceptible to SARS-CoV-2, the researchers had to use genetically adapted mice, able to generate the SARS-CoV-2 binding protein Angiotensin Converting Enzyme 2 (ACE2). “The mouse model we used recapitulates key aspects of the human COVID-19 disease,” added Prof. Hiroki Kato from the Institute of Cardiovascular Immunology at the UKB.
Using this model, the researchers of the University Hospital Bonn could show that a systemic application of 3pRNA, one to seven days prior to infection with SARS-CoV-2, drastically reduced the proportion of lethal infections. A similar observation was made for therapeutic application of 3pRNA, one day after infection. “Our findings clearly show that targeting RIG-I, both in a prophylactic and a therapeutical manner, is a promising approach in the treatment of COVID-19. However, prior to application in humans, further studies need to be conducted,” summarized Prof. Gunther Hartmann from the Institute of Clinical Chemistry and Clinical Pharmacology and speaker of the Cluster of Excellence ImmunoSensation2.
Participating institutions and funding
In addition to the Institute of Clinical Chemistry and Clinical Pharmacology, the Institute of Virology, the Institute of Cardiovascular Immunology and the Mildred Scheel School of Oncology at the University Hospital Bonn, the German Center for Infection Research and the Institute of Tropical Medicine, Antwerpen, Belgium were involved. The study was mainly funded by the German Research Foundation (DFG).
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