May 30, 2017 These cross-section images show three-dimensional human skin models made of living skin cells. Untreated model skin (left panel) shows a thinner dermis layer (black arrow) compared with model skin treated with the antioxidant methylene blue (right panel). A new study suggests that methylene blue could slow or reverse dermal thinning (a sign of aging) and a number of other symptoms of aging in human skin. Credit: Zheng-Mei Xiong/University of Maryland

New work from the University of Maryland suggests that a common, inexpensive and safe chemical could slow the aging of human skin. The researchers found evidence that the chemicalan antioxidant called methylene bluecould slow or reverse several well-known signs of aging when tested in cultured human skin cells and simulated skin tissue. The study was published online in the journal Scientific Reports on May 30, 2017.

"Our work suggests that methylene blue could be a powerful antioxidant for use in skin care products," said Kan Cao, senior author on the study and an associate professor of cell biology and molecular genetics at UMD. "The effects we are seeing are not temporary. Methylene blue appears to make fundamental, long-term changes to skin cells."

The researchers tested methylene blue for four weeks in skin cells from healthy middle-aged donors, as well as those diagnosed with progeriaa rare genetic disease that mimics the normal aging process at an accelerated rate. In addition to methylene blue, the researchers also tested three other known antioxidants: N-Acetyl-L-Cysteine (NAC), MitoQ and MitoTEMPO (mTEM).

In these experiments, methylene blue outperformed the other three antioxidants, improving several age-related symptoms in cells from both healthy donors and progeria patients. The skin cells (fibroblasts, the cells that produce the structural protein collagen) experienced a decrease in damaging molecules known as reactive oxygen species, a reduced rate of cell death and an increase in the rate of cell division throughout the four-week treatment.

Next, Cao and her colleagues tested methylene blue in fibroblasts from older donors (>80 years old) again for a period of four weeks. At the end of the treatment, the cells from older donors had experienced a range of improvements, including decreased expression of two genes commonly used as indicators of cellular aging: senescence-associated beta-galactosidase and p16.

"I was encouraged and excited to see skin fibroblasts, derived from individuals more than 80 years old, grow much better in methylene blue-containing medium with reduced cellular senescence markers," said Zheng-Mei Xiong, lead author of the study and an assistant research professor of cell biology and molecular genetics at UMD. "Methylene blue demonstrates a great potential to delay skin aging for all ages."

The researchers then used simulated human skin (a system developed by Cao and Xiong) to perform several more experiments. This simulated skina three-dimensional model made of living skin cellsincludes all the major layers and structures of skin tissue, with the exception of hair follicles and sweat glands. The model skin could also be used in skin irritation tests required by the Food and Drug Administration for the approval of new cosmetic products, Cao said.

"This system allowed us to test a range of aging symptoms that we can't replicate in cultured cells alone," Cao said. "Most surprisingly, we saw that model skin treated with methylene blue retained more water and increased in thicknessboth of which are features typical of younger skin."

The researchers also used the model skin to test the safety of cosmetic creams with methylene blue added. The results suggest that methylene blue causes little to no irritation, even at high concentrations. Encouraged by these results, Cao, Xiong and their colleagues hope to develop safe and effective ways for consumers to benefit from the properties of methylene blue.

"We have already begun formulating cosmetics that contain methylene blue. Now we are looking to translate this into marketable products," Cao said. "We are also very excited to develop the three-dimensional skin model system. Perhaps down the road we can customize the system with bioprinting, such that we might be able to use a patient's own cells to provide a tailor-made testing platform specific to their needs."

The research paper, "Anti-Aging Potentials of Methylene Blue for Human Skin Longevity," Zheng-Mei Xiong, Mike O'Donovan, Linlin Sun, Ji Young Choi, Margaret Ren and Kan Cao, was published online in the journal Scientific Reports on May 30, 2017.

Explore further: Safe, inexpensive chemical found to reverse symptoms of progeria in human cells

More information: Zheng-Mei Xiong et al, Anti-Aging Potentials of Methylene Blue for Human Skin Longevity, Scientific Reports (2017). DOI: 10.1038/s41598-017-02419-3

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Common antioxidant could slow symptoms of aging in human skin - Medical Xpress

The chemistry of cells is essentially the chemistry of carbon-containing compounds because the carbon atom has several unique properties that make it especially suitable as the backbone of biologically important molecules. To study cellular molecules really means to study carbon-containing compounds. Almost without exception, molecules of importance to the cell biologist have a backbone, or skeleton, of carbon atoms linked together covalently.

Actually, the study of carbon-containing compounds is the domain of organic chemistry. In its early days, organic chemistry was almost synonymous with biological chemistry because most of the carboncontaining compounds that chemists first investigated were obtained from biological sources (hence the word organic, acknowledging the organismal origins of the compounds).

The terms have long since gone their separate ways, however, because organic chemists have now synthesised an incredible variety of carbon-containing compounds that do not occur naturally (that is, not in the biological world). Organic chemistry therefore includes all classes of carbon-containing compounds, whereas biological chemistry (biochemistry for short) deals specifically with the chemistry of living systems and is, as we have already seen, one of the several historical strands that form an integral part of modern cell biology.

The carbon atom is the most important in biological molecules. The diversity and stability of carbon-containing compounds are due to specific properties of the carbon atom and especially to the nature of the interactions of carbon atoms with one another as well as with a limited number of other elements found in molecules of biological importance.

The single most fundamental property of the carbon atom is its valence of four, which means that the outermost electron orbital of the atom lacks four of the eight electrons needed to fill it completely. Since a complete outer orbital is required for the most stable chemical state of an atom, carbon atoms tend to associate with one another or with other electrondeficient atoms, allowing adjacent atoms to share a pair of electrons. For each such pair, one electron comes from each of the atoms. Atoms that share each others electrons in this way are said to be joined together by a covalent bond. Carbon atoms are most likely to form covalent bonds with one another and with atoms of oxygen, hydrogen, nitrogen, and sulphur.

The electronic configurations of several of these atoms are such that in each case, one or more electrons are required to complete the outer orbital. The number of missing electrons corresponds in each case to the valence of the atom, which indicates, in turn, the number of covalent bonds the atom can form. Carbon, oxygen, hydrogen, and nitrogen are the lightest elements that form covalent bonds by sharing electron pairs. This lightness, or low atomic weight, makes the resulting compounds especially stable, because the strength of a covalent bond is inversely proportional to the atomic weights of the elements involved in the bond.

Because four electrons are required to fill the outer orbital of carbon, stable organic compounds have four covalent bonds for every carbon atom. Methane, ethanol, and methylamine are simple examples of such compounds, containing only single bonds between atoms. Sometimes, two or even three pairs of electrons can be shared by two atoms, giving rise to double bonds or triple bonds. Ethylene and carbon dioxide are examples of doublebonded compounds. Triple bonds are found in molecular nitrogen and hydrogen cyanide. Thus, both its valence and its low atomic weight confer on carbon unique properties that account for the diversity and stability of carbon-containing compounds and give it a preeminent role in biological molecules.

The writer is associate professor, head, department of botany, ananda mohan college, kolkata, and also fellow, botanical society of bengal, and can be contacted at tapanmaitra59@yahoo.co.in

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The importance of carbon - The Statesman

Physicist Stephen Hawking is perhaps the most famous sufferer of motor neuron disease, a crippling degenerative condition that affects an estimated 150,00 people around the world.

Karwai Tang / Getty

In news that may bring hope to Stephen Hawking and hundreds of thousands of others around the world, British scientists have used reprogrammed skin cells to study the development of motor neuron disease.

Its like changing the postcode of a house without actually moving it, explains neuroscientist Rickie Patani, referring to research offering startling new insights into the progress and treatment of the crippling degenerative condition, also known as amyotrophic lateral sclerosis (ALS).

Patani, together with colleague Sonia Gandhi, both from the Francis Crick Institute and University College London, in the UK, led a team of researchers investigating how the disease destroys the nerve cells that govern muscle movement.

The results, published in the journal Cell Reports, comprise the most fine-grained work to date on how ALS operates on a molecular level and suggest powerful new treatment methods based on stem cells.

Indeed, so exciting are the implications of the research that Ghandi and Patani are already working with pharmaceutical companies to develop their discoveries.

The neurologists uncovered two key interlinked interactions in the development of motor neuron disease, the first concerning a particular protein, and the second concerning an auxiliary nerve cell type called astrocytes.

To make their findings, the team developed stem cells from the skin of healthy volunteers and a cohort carrying a genetic mutation that leads to ALS. The stem cells were then guided into becoming motor neurons and astrocytes.

We manipulated the cells using insights from developmental biology, so that they closely resembled a specific part of the spinal cord from which motor neurons arise, says Patani.

We were able to create pure, high-quality samples of motor neurons and astrocytes which accurately represent the cells affected in patients with ALS."

The scientists then closely monitored the two sets of cells healthy and mutated to see how their functioning differed over time.

The first thing they noted was that a particular protein TDP-43 behaved differently. In the patient-derived samples TDP-43 leaked out of the cell nucleus, catalysing a damaging chain of events inside the cell and causing it to die.

The observation provided a powerful insight into the molecular mechanics of motor neuron disease.

Knowing when things go wrong inside a cell, and in what sequence, is a useful approach to define the critical molecular event in disease, says Ghandi.

One therapeutic approach to stop sick motor neurons from dying could be to prevent proteins like TDP-43 from leaving the nucleus, or try to move them back.

The second critical insight was derived from the behaviour of astrocytes, which turned out to function as a kind of nursemaid, supporting motor neuron cells when they began to lose function because of protein leakage.

During the progression of motor neuron disease, however, the astrocytes like nurses during an Ebola outbreak eventually fell ill themselves and died, hastening the death of the neurons.

To test this, the team did a type of mix and match exercise, concocting various combinations of neurons and astrocytes from healthy and diseased tissue.

They discovered that healthy astrocytes could prolong the functional life of ALS-affected motor neurons, but damaged astrocytes struggled to keep even healthy motor neurons functioning.

The research reveals both TDP-43 and astrocytes as key therapeutic targets, raising the possibility that the progress of ALS might be significantly slowed, or perhaps even halted.

Our work, along with other studies of ageing and neurodegeneration, would suggest that the cross-talk between neurons and their supporting cells is crucial in the development and progression of ALS, says Patani.

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Patients' stem cells point to potential treatments for motor neuron disease - Cosmos

Courtesy of UCR Today

On May 10, Jun-Hyeong Cho, assistant professor of cell biology and neuroscience at UCR, and Woong Bin Kim, a postdoctoral researcher in Chos lab, published their study on fear memory in Journal of Neuroscience. Cho and Kim conducted studies on fear memory to understand how the brain interprets and remembers fear. They concluded that humans and animals develop adaptive fear responses to dangerous situations to survive. In addition, their research focused on the specific areas of the brain that are involved in fear memory.

Their study focused on understanding the mechanistic features of the double-projecting neurons that are sent out from the hippocampus to the amygdala and the medial prefrontal cortex (mPFC). The hippocampus encodes context cues (the set of circumstances around an event), the amygdala stores associations between a context and an aversive event, and the mPFC signals whether a defensive response is appropriate in the present context, Cho explained in an interview with the Highlander.

This study could help researchers learn more about fear-related conditions such as post-traumatic stress disorder (PTSD). According to the U.S. Department of Veterans Affairs, PTSD is a mental health problem that some people develop after experiencing or witnessing a life-threatening event, like combat, a natural disaster, a car accident, or sexual assault. Cho explained that around seven percent of Americans today suffer from PTSD, and this study proposes that it may be caused by a disruption in the natural fear-learning process.

To conduct their research, the pair used a tracing method in the brains of the mice to show the hippocampal neurons that project to different areas in the brain. The neurons are labeled with fluorescent proteins with different colors to show their movements throughout the brain. We also found neural mechanisms (are) how these double-projecting neurons efficiently convey contextual information to the amygdala and mPFC to encode and retrieve fear memory for a context associated with an aversive event, said Cho.

Cho has been an assistant professor in the cell biology and neuroscience department at UCR since 2014. Before coming to UCR, Cho was an instructor in psychiatry at Harvard Medical School from 2012-2014. Cho hopes that his continued research will uncover how the brain works in learning and fear.

Cho says that they want to continue researching about the effects of these neurons on individuals fear memory. To do this, they will selectively silence the neurons and see how it impacts the formation of fear memory. Although the two researchers have published their work so far, they hope to continue research in this field in the future.

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UCR researchers explore how the brain communicates fear - Highlander Newspaper

Cell biology is the study of processes carried out by individual cells such as cell division, organelle inheritance and biogenesis, signal transduction and motility. These processes are often affected by stimuli from the environment including nutrients, growth signals, and cell-cell contact. Single-celled organisms such as yeast, multicellular organisms such as Drosophila and mouse, established tissue culture lines, and, increasingly, primary cell cultures derived from recombinant animals such as mice are commonly used to study cell biological problems. Experimental approaches to the study of cell biological problems include genetics, microscopy, and reconstitution of cell biological events in cell-free systems.

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Cell Biology | MIT Biology

In diseases like cancer, diabetes, rheumatism and stroke, a disorder develops in the blood vessels that exacerbates the condition and obstructs treatment. Researchers at Karolinska Institutet now show how blood vessels can normally change their size to create a functional circulatory system and how vascular malformation during disease can occur. In the study, published in Nature Cell Biology, the researchers managed to treat vascular malformation in mice, a discovery of potential significance to numerous vascular diseases.

A healthy body has a perfect balance of arteries, capillaries and veins that allow the blood to reach every cell in the body and that form what is called the vascular tree. New blood vessels are formed by endothelial cells, which normally coat the inside of blood vessels and which organise themselves into tubes and mature, along with other cells, into arteries, capillaries or veins.

Throughout a persons life, the vascular tree has to adapt its branches to the changing needs of body tissue, such as during growth, muscle building or wound healing. However, there are diseases that affect the endothelial cells in a way that throws the vascular tree out of balance, which exacerbates the disease and often causes haemorrhaging. In cancer, for example, it is known that the vessels leak and direct shunts form between arteries and veins, preventing drugs from reaching the tumour.

To understand how arteries, veins and capillaries are created and how the process malfunctions in the presence of disease the researchers studied normal vascular formation and the inherited Osler-Weber-Rendu disease (HHT), which is characterised by vascular malformation and repeated haemorrhaging, with an increased risk of stroke. By switching signals on and off in the endothelial cells of genetically manipulated mice, the researchers could describe how the protein Endoglin controls vascular formation and malformation. They found that the protein acts like a sensor that detects blood flow and tells the endothelial cells to organise themselves into veins, capillaries or arteries as necessary. Cells that lacked the protein were less able to form arteries.

The researchers were also able to reduce vascular malformation in the genetically manipulated mice.

Our findings contribute to the understanding of fundamental biological processes that explain how the vascular tree is formed and what causes vascular malformation, says Lars Jakobsson, assistant professor at Karolinska Institutets Department of Medical Biochemistry and Biophysics. Drugs with a similar effect as one of those we tested are currently used to treat patients with inherited vascular malformation but are still under evaluation. Now we have another candidate and a more nuanced idea of how it works. We are now in a better position to control the formation and malformation of blood vessels and thus their function, which can eventually lead to improved treatments for a number of diseases.

The researchers at Karolinska Institutet also contributed to a parallel study, published in the same issue of Nature Cell Biology, describing how blood flow influences endothelial cell size that in turn affects vessel identity and malformation.

This article has been republished frommaterialsprovided byKarolinska Institutet. Note: material may have been edited for length and content. For further information, please contact the cited source.

Publications

Endoglin prevents vascular malformation by regulating flow-induced cell migration and specification through VEGFR2 signalling. Yi Jin, LarsMuhl, Mikhail Burmakin, YixinWang, Anne-Claire Duchez, Christer Betsholtz, Helen M. Arthur and Lars Jakobsson. Nature Cell Biology, online 22 May 2017

Endoglin controls blood vessel diameter through endothelial cell shape changes in response to haemodynamic cues. Wade W. Sugden, RobertMeissner, Tinri Aegerter-Wilmsen, Roman Tsaryk, Elvin V. Leonard, Jeroen Bussmann, Mailin J. Hamm, Wiebke Herzog, Yi Jin, Lars Jakobsson, Cornelia Denz, Arndt F. Siekmann. Nature Cell Biology, online 22 May 2017

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New Insights into how the Vascular Tree is Formed - Technology Networks

May 25, 2017 Researchers at Howard Hughes Medical Institute developed a way to produce color-tagged, 3D, microscopic videos of organelles in a live cell. They came to Drexel's Andrew Cohen, PhD, to develop an algorithm that could process massive amounts of visual data to better understand the behavior of organelles as a group and individually. This technology will help them unlock cell behavior and response to drug treatment. Credit: Drexel University

Researchers at Howard Hughes Medical Institute and the Eunice Kennedy Shriver National Institute for Child Health and Human Development are getting a first glimpse at the inner-workings of live cells thanks to a new microscopy technique pioneered by Nobel laureate Eric Betzig with help from engineers at Drexel University. Their method uses grids of light that activate fluorescent color tags on each type of organellethe result is a 3-D video that gives researchers their best look at how cells function. It will allow scientists to better understand how cells react to environmental stressors and respond to drug treatment.

In a paper published today in Nature, the team lays out its methodology for using Betzig's lattice light sheet microscope in combination with image-tracking technology developed in Drexel's Computational Image Sequence Analysis Lab, led by Andrew Cohen, PhD, to produce 3-D time lapse videos of organelle movement and generate quantitative data on their interactions.

"The cell biology community has recognized for many years that the cytoplasm is full of many different types of organelles, and the field is recognizing more and more how significant cross-talk between these organelles is in the form of close contacts between these organelles," said Jennifer Lippincott-Schwartz, PhD, of HHMI's Janelia Research Campus, and senior author of the study. "When two organelles come close to each other they can transfer small molecules like lipids and calcium and communicate with each other through that transfer. But no one has been able to look at the whole set of these interactions at any particular time. This technology is providing a way to do that. But this paper is about a whole new technology, being able to tag six different objects with six different fluorophores, and unmixing the fluorophores so that you can observe the six different objects discretely."

Betzig's microscopy technique uses layers of light grids that interact with fluorescent protein-tagged cells to build a 3D microscopic image. At Janelia Research Campus, Betzig and Lippincott-Schwartz have refined that technology to produce a detailed look inside the cell by tagging each organelle type with its own color.

"The challenge is analyzing this data," Lippincott-Schwartz said. "It requires being able to simultaneously track these six different objects in 3D. What Andy Cohen and his group have done with the software system they have developed is enable us to really look at this in more quantitative ways than would be possible with conventional tools."

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Cohen's lab developed a tool called LEVER 3-D in 2015 to help researchers study 3-D images of neural stem cells. It applies an advanced image segmentation algorithm they developed that can identify boundaries of cells and track their movements. Prior to this technology being available to microbiologists, the processing of microscopic images and time-lapse footage would take massive amounts of time because they would have to create lineage trees by hand and attempt to follow cell changes by making their own observations when comparing images.

This process is even more involved when multiple objects are being tracked in three dimensions. Lippincott-Schwartz's group used a battery of computer programs to filter out all the different pieces of light spectra emitted by the organelles, to begin to bring the 3-D images and video into focus. The process, called "linear unmixing," required more than 32 cores of a computer work station to sift through 7 billion sets of six-color images, pixel by pixel.

Typically they would use expensive commercial software programs to stitch them into a 3-D volume to go about studying them. But these programs are expensive and time-consuming to use, and were not capable of the sophisticated analysis for tracking moving objects in order to make quantitative measurements of their behaviors and particularly how they interact.

Cohen's algorithm automates the entire process, which saves researchers a lot of time and it also lets them ask and answer more questions about what the cells are doing. He further verified the data by working with Drexel colleague Uri Herschberg, PhD, an associate professor in the School of Biomedical Engineering, Science and Health Systems and College of Medicine, to check it against 2-D images of the cells.

"It's some really impressive footage that gives biologists this ability to look deeper and deeper into live cells and see things they've never seen beforelike six different organelles in a living cell in true 3-D," said Cohen, a professor in Drexel's College of Engineering. "But it's also a lot of work to begin quantifying what they're seeingand that's where we can help, by using our program to automate big portions of that process and glean valuable data from it."

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Using the new technology to simultaneously look at six sets of organelles, Lippincott-Schwartz's teams at Janelia and at the National Institutes of Health are making exciting new observations. They are looking at how the organelles distribute themselves inside the cell, how often they interact with each other and where, when and how fast they move during various times in the cell's lifecycle.

"One very interesting outcome is that we found the largest organelle in the cell, which is the ER [endoplasmic reticulum], at any particular time point will be occupying about 25 percent of the volume of the cytoplasm, excluding the nucleus. But if you track the way it disperses through the cytoplasm over a short period of time, like 15 minutes, you see that it explores 95 percent of the whole cytoplasm during that time period," Lippincott-Schwartz said. "We can do this for all of the other organelles at the same time to see how the cytoplasm is being sensed through the dynamic motions of dispersive activities of these organelles."

Observing sub-cellular behavior is just the first application of this technology. Now that it has proven to generate usable data, the team will forge ahead to study what happens inside a cell when it is exposed to drug treatments and other common stresses on the system. The researchers suggest that it could be used to study many more than six types of microscopic objects. And it could help dig even deeper into the building blocks of lifeinto interactions of RNA particles and other proteins that play a role in a cell's function and the behavior of diseased cells.

"As these tools continue to improve they will give researchers both a better look at cell behavior and many options for gathering and analyzing that data," Cohen said. "They will be able to ask and answer increasingly complicated questions and that's going to lead to some very exciting and important discoveries."

Explore further: How plant cell compartments change with cell growth

More information: Alex M. Valm et al. Applying systems-level spectral imaging and analysis to reveal the organelle interactome, Nature (2017). DOI: 10.1038/nature22369

Journal reference: Nature

Provided by: Drexel University

A research team led by Kiminori Toyooka from the RIKEN Center for Sustainable Resource Science has developed a sophisticated microscopy technique that for the first time captures the detailed movement of subcellular organelles ...

(Phys.org)A team of researchers from the U.S. and the U.K. has used high-resolution imaging techniques to get a closer look at the endoplasmic reticulum (ET), a cellular organelle, and in so doing, has found that its structure ...

For hundreds of years biologists have studied cells through the lens of a microscope. With a little help from a team of engineers at Drexel University, these scientists could soon be donning 3-D glasses in a home-theater-like ...

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Researchers at the University of Iowa have discovered that a molecule which can sense the swelling of fat cells also controls a signaling pathway that allows fat cells to take up and store excess glucose. Mice missing this ...

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Living cells must constantly process information to keep track of the changing world around them and arrive at an appropriate response.

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Researchers help provide first glimpse of organelles in action inside living cells - Phys.Org

Researchers from Princeton Universitys Department of Molecular Biology have identified a small RNA molecule that helps maintain the activity of stem cells in both healthy and cancerous breast tissue. The study, which will be published in the June issue of Nature Cell Biology, suggests that this microRNA promotes particularly deadly forms of breast cancer and that inhibiting the effects of this molecule could improve the efficacy of existing breast cancer therapies.

Stem cells give rise to the different cell types in adult tissues but, in order to maintain these tissues throughout adulthood, stem cells must retain their activity for decades. They do this by self-renewing dividing to form additional stem cells and resisting the effects of environmental signals that would otherwise cause them to prematurely differentiate into other cell types.

Many tumors also contain so-called cancer stem cells that can drive tumor formation. Some tumors, such as triple-negative breast cancers, are particularly deadly because they contain large numbers of cancer stem cells that self-renew and resist differentiation.

To identify factors that help non-cancerous mammary gland stem cells (MaSCs) resist differentiation and retain their capacity to self-renew, Yibin Kang, the Warner-Lambert/Parke-Davis Professor of Molecular Biology, and colleagues searched for short RNA molecules called microRNAs that can bind and inhibit protein-coding messenger RNAs to reduce the levels of specific proteins. The researchers identified one microRNA, called miR-199a, that helps MaSCs retain their stem-cell activity by suppressing the production of a protein called LCOR, which binds DNA to regulate gene expression. The team showed that when they boosted miR-199a levels in mouse MaSCs, they suppressed LCOR and increased normal stem cell function. Conversely, when they increased LCOR levels, they could curtail mammary gland stem cell activity.

Kang and colleagues found that miR-199a was also expressed in human and mouse breast cancer stem cells. Just as boosting miR-199a levels helped normal mammary gland stem cells retain their activity, the researchers showed that miR-199a enhanced the ability of cancer stem cells to form tumors. By increasing LCOR levels, in contrast, they could reduce the tumor-forming capacity of the cancer stem cells. In collaboration with researchers led by Zhi-Ming Shao, a professor at Fudan University Shanghai Cancer Center in China, Kangs team found that breast cancer patients whose tumors expressed large amounts of miR-199a showed poor survival rates, whereas tumors with high levels of LCOR had a better prognosis.

Kang and colleagues found that LCOR sensitizes cells to the effects of interferon-signaling molecules released from epithelial and immune cells, particularly macrophages, in the mammary gland. During normal mammary gland development, these cells secrete interferon-alpha to promote cell differentiation and inhibit cell division, the researchers discovered. By suppressing LCOR, miR-199a protects MaSCs from interferon signaling, allowing MaSCs to remain undifferentiated and capable of self-renewal.

The microRNA plays a similar role during tumorigenesis, protecting breast cancer stem cells from the effects of interferons secreted by immune cells present in the tumor. This is a very nice study linking a normal and malignant mammary gland stem cell program to protection from immune modulators, said Michael Clarke, the Karel H. and Avice N. Beekhuis Professor in Cancer Biology at Stanford School of Medicine, Institute of Stem Cell Biology and Regenerative Medicine, who first discovered breast cancer stem cells but was not involved in this study. It clearly has therapeutic implications for designing strategies to rationally target the breast cancer stem cells with immune modulators.

Toni Celi-Terrassa, an associate research scholar in the Kang lab and the first author of the study, said, This study unveils a new property of breast cancer stem cells that give them advantages in their interactions with the immune system, and therefore it represents an excellent opportunity to exploit for improving immunotherapy of cancer.

Interferons have been widely used for the treatment of multiple cancer types, Kang said. These treatments might become more effective if the interferon-resistant cancer stem cells can be rendered sensitive by targeting the miR-199a-LCOR pathway.

This article has been republished frommaterialsprovided byPrinceton University. Note: material may have been edited for length and content. For further information, please contact the cited source.

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RNA Molecule that Shields Breast Cancer Stem Cells from Immune System Identified - Technology Networks

May 25, 2017

Researchers at the University of Iowa have discovered that a molecule which can sense the swelling of fat cells also controls a signaling pathway that allows fat cells to take up and store excess glucose. Mice missing this protein, known as SWELL1, gain less weight (fat) than normal mice on a high-fat diet, but also develop diabetes.

"Although we have created a mouse that is resistant to weight gain by removing the SWELL1 protein, the mouse is not healthy; it has insulin resistance and glucose intolerance," says Rajan Sah, MD, PhD, assistant professor of internal medicine at the University of Iowa Carver College of Medicine and senior author of the study.

Type 2 diabetes is one of the more serious health problems associated with obesity. The disease makes cells less sensitive to insulin and causes blood sugar levels to become abnormally high. It is healthier for the body to store excess glucose as fat rather than have it circulating in the blood where it can damage blood vessels and nerves.

In healthy people, insulin released in response to high glucose levels acts on many different tissues to coordinate use or storage of the glucose. It triggers fat cells to take up excess glucose and store it as fat.

Sah's study, which was published recently in Nature Cell Biology, found that removing SWELL1 from fat cells in mice disrupts this insulin signaling pathway and prevents fat cells from taking up glucose.

Sah and his team homed in on SWELL1 because of several pieces of converging evidence. Fat cells have a tremendous capacity to expand - up to 30 times their normal volume in the context of obesity. It's also long been known that changes in fat cell size alters fat cell signaling.

Through exploratory experiments investigating cell swelling in fat cells from lean and obese mice as well as fat cells obtained from bariatric surgery patients, Sah and his team serendipitously identified SWELL1 protein as an essential component of fat cells' volume-sensing mechanism. From unrelated work by other researchers, they also knew that this protein was involved in a signaling pathway common to all cells. In fat cells this pathway regulates glucose uptake in response to insulin.

"We thought maybe this SWELL1 protein is what links the two pieces together - the size-sensing mechanism and the signaling pathway that responds to size changes by altering insulin sensitivity," explains Sah, who also is a member of the Fraternal Order of Eagles Diabetes Research Center, and the Abboud Cardiovascular Research Center at the UI.

The team's study showed that swelling of mouse or human fat cells, either artificially in a petri dish, or because the cells have expanded due to obesity, activates SWELL1 signaling. Removing SWELL1 from mouse fat cells knocks out this volume-sensing signal and disrupts the insulin signaling pathway used by fat cells to take up and store excess glucose. Mice missing SWELL1 have smaller fat cells, but also develop insulin resistance and glucose intolerance.

Interestingly, on a regular diet, mice missing SWELL1 had body weights, fat composition, and metabolism that were all essentially the same as a normal mouse. The only difference was they had no SWELL1 activity in their fat cells, as well as reduced ability to clear glucose from the blood and impaired insulin sensitivity (insulin resistance).

When the mice were put on a high-fat diet, the mice missing SWELL1 did not gain weight as fast as the normal mice but the insulin resistance and glucose intolerance became worse.

"The idea that fat is bad is not necessarily true," Sah says. "Too much fat is bad, and fat in the wrong places is bad, but fat in the right place and allowed to expand normally may be somewhat protective against diabetes.

"If fat cells can sense their own expansion, then SWELL1 protein might be the mechanism for that," he continues. "What we see here is what the cell does with the information that it is getting bigger. It turns on a signaling pathway that modulates glucose uptake and insulin sensitivity. From this discovery, we can start to look at whether we can target this modulation of insulin sensitivity in a therapeutic way."

Explore further: Your muscles can 'taste' sugar, research finds

More information: Yanhui Zhang et al, SWELL1 is a regulator of adipocyte size, insulin signalling and glucose homeostasis, Nature Cell Biology (2017). DOI: 10.1038/ncb3514

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Living cells must constantly process information to keep track of the changing world around them and arrive at an appropriate response.

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Can fat 'feel' fat? Size-sensing protein controls glucose uptake and storage in fat cells - Phys.Org

The best part of high school biology was the movies. Some of them basically amounted to weird close-up fetish porn, sure. Other high school biology videos were actually educational, including the only one that ever taught me anything about the human cell, Inner Life of a Cell. But a new video puts them all to shame.

Rather than using boring old computer-generated graphics, a team of American scientists made what might be the most complex video of a cell in action yet. Its all based on a real monkey cell, analyzed with a series of proteins, dyes and a special kind of microscope.

Sure, other microscopes have made videos of cells moving, or pairs of cell parts, called organelles, interacting. But this is the first time were doing this many compartments in live cells, Sarah Cohen, scientist at the National Institutes of Health, told Gizmodo.

The video shows the chaotic movement of lipid (fat) droplets traveling through different parts of the cell. You might remember that the cell is a factory, where the mitochondria is the power plant. The endoplasmic reticulum makes stuff like proteins and lipids, and the golgi apparatus packages them. The lysosomes and peroxisomes break things down. Now, you can see all those organelles doing their jobs simultaneously, thanks to the research published today in the journal Nature.

Getting such a detailed look at the cells function was surprisingly intuitive. The researchers tagged the different organelles with proteins that fluoresce in response to different colors of light. They also soaked the cell in a dye that sticks to lipid molecules so they could visualize how they traveled between organelles. A special microscope looks at the cell in slices, rather than viewing the entire thing at once, which prevents the light from killing it. The study added evidence that the endoplasmic reticulum serves as the central hub of the cell, and looks like a mesh, interacting with nearly everything else.

Other researchers are excited about the new tool. [The study authors] breakthrough opens up wide-ranging opportunities for exploring the molecular mechanisms that underpin the organelle communitys dance, Sang-Hee Shim, assistant chemistry professor at Korea University wrote in commentary for Nature.

Like any scientific method, there are limitations to this one. Too much time under the microscope could harm the cell, for example. Plus, the resolution isnt as good as more invasive microscope techniques, so it might muddle some of the finer details, like the interaction point between the mitochondrion and the endoplasmic reticulum, said Shim.

But the method will definitely help scientists figure out exactly how the cell works and how molecules move around inside of it. This could be useful for things like drug screening or personalized medicine, applications where you need to know exactly where and how a molecule is moving down to the cellular level, said Cohen.

Really, its just cool as hell.

[Nature]

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This Is the Most Complex Video of a Real Cell Ever Made - Gizmodo