June 6, 2017 First author Angela Arensdorf, Ph.D., and corresponding author Stacey Ogden, Ph.D., an associate member of the St. Jude Department of Cell and Molecular Biology. Credit: Peter Barta / St. Jude Children's Research Hospital

St. Jude Children's Research Hospital molecular biologists have identified an enzyme that activates and "supercharges" cellular machinery that controls how cells become specialized cells in the body.

Malfunction of that machinery, dubbed the Sonic Hedgehog pathway, causes a variety of developmental disorders and cancers, including childhood medulloblastoma and basal cell carcinoma. Researchers believe their basic discovery opens a new research pathway that could lead to drugs to treat such disorders.

Led by Stacey Ogden, Ph.D., an associate member of the St. Jude Department of Cell and Molecular Biology, the research was published June 6 in the journal Cell Reports.

The scientific puzzle the researchers sought to understand was how a major activator of the Sonic Hedgehog pathway, called Smoothened, manages to make its way into an antenna-like cell structure called a "primary cilium," where it communicates with its downstream signaling partners.

Every cell in the body sprouts a primary cilium, which harbors a whole factory of cellular machinery that the cell uses to translate external stimuli into cell responses. Such stimuli include mechanical movement and chemical signals such as hormones. Normally, Smoothened is barred from the primary cilium, keeping the Sonic Hedgehog pathway safely controlled.

In their experiments with cell cultures, the researchers discovered that an enzyme called Phospholipase A2 triggers a mechanism that opens the way for Smoothened movement into the cilium. What's more, the phospholipase triggers an amplification that "supercharges" Smoothened signaling.

"We've basically revealed a new layer of regulation of Smoothened trafficking," Ogden said. "This is a very hot area of research now, because Smoothened trafficking appears to be a very crucial control point for signaling activity. So, if you can change Smoothened trafficking, you can very easily adjust the amplitude of Sonic Hedgehog signaling."

The basic finding has potential clinical importance, Ogden said, because reduced activity in the Sonic Hedgehog pathway is commonly found in genetic disorders of primary cilia function. These disorders include Joubert syndrome, Bardet-Biedl syndrome, Ellis van Creveld syndrome and polycystic kidney diseaseone of the most common genetic diseases in the U.S., affecting more than 600,000 people. Better understanding of the control machinery for the Sonic Hedgehog pathway could lead to more effective therapies for the disorders, Ogden said.

Conversely, hyperactivity of the Sonic Hedgehog pathway is the cause of about 30 percent of childhood medulloblastomas. Medulloblastoma is the most common malignant brain tumor of childhood, accounting for about 20 percent of all childhood brain tumors. Current treatments using surgery, radiation and chemotherapy cause severe side effects, so more precise drug treatments are urgently needed.

"One of the drugs now being used to treat medulloblastoma is a Smoothened inhibitor," Ogden said. "But tumor cells frequently become resistant to this drug and begin to grow again because of mutations in Smoothened that enable it to overcome the drug's inhibition. We want to determine whether drugs to inhibit Phospholipase A2 could reduce Sonic Hedgehog activity in cases where Smoothened becomes insensitive to targeted inhibition."

In adults, Hedgehog pathway hyperactivation also causes basal cell carcinoma, the most common skin cancer and one of the most common cancers. Hedgehog pathway activation also may accelerate other types of tumors by affecting the tissue surrounding the tumor, called the stroma, to create an environment more conducive to growth, Ogden said.

"So Hedgehog pathway inhibitors may be useful in combination therapies with other traditional chemotherapies for other types of solid tumors," she said.

In further research, Ogden and her colleagues are continuing to examine Smoothened regulation and exploring drugs that affect its activity.

Explore further: Blocking a protein in a critical signaling pathway could offer a new way to combat tumors

Cancer drugs that block a cell-signaling pathway called Hedgehog have shown promise in recent years in treating patients with skin cancer, leukemia and other types of tumors. But the available treatments mostly target the ...

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St. Jude Children's Research Hospital molecular biologists have identified an enzyme that activates and "supercharges" cellular machinery that controls how cells become specialized cells in the body.

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Santa Cruz, CA (Scicasts) The DNA vital to the life of a cell is packaged in chromosomes, and a variety of checkpoints, repair mechanisms, and other cellular safeguards exist to maintain the integrity of the chromosomes during cell growth and division. Those safeguards can fail, however, and a cell may find itself trying to divide into two daughter cells with a loose chromosomal fragment drifting away from a broken chromosome.

William Sullivan calls this a "worst case scenario" for the cell. The potential consequences include cell death or a cancerous cell growing out of control. But Sullivan, a professor of molecular, cell, and developmental biology at UC Santa Cruz, has found that the cell still has one more trick up its sleeve to rescue the broken chromosome.

The latest findings from Sullivan's lab, published in the June 5 issue of Journal of Cell Biology, reveal new aspects of a remarkable mechanism that carries broken chromosomes through the process of cell division so that they can be repaired and function normally in the daughter cells. Sullivan has been studying this process in the fruit fly Drosophila melanogaster. His lab has created a strain of flies in which broken chromosomes are common due to the expression of a DNA-cutting enzyme.

"We have flies in which 80 percent of the cells have double-strand breaks in the DNA, and the flies are fine," he said. "The cell has this amazing mechanism, like a Hail Mary pass with time running out."

The mechanism involves the creation of a DNA tether which acts as a lifeline to keep the broken fragment connected to the chromosome. Powerful new microscopy techniques enable researchers to observe the whole process in living cells, with bright fluorescent tags highlighting the chromosomes and other cellular components.

When a cell divides, it duplicates its chromosomes to make one set for each of the daughter cells. The membrane around the nucleus, which keeps the chromosomes separate from the rest of the cell, breaks down. The two sets of chromosomes then line up and segregate to opposite sides of the cell, pulled apart by a structure of microtubules called the spindle. A new nuclear envelope forms around each set of chromosomes, and new cell membranes separate the two daughter cells.

Sullivan's research has shown that chromosome fragments don't segregate with the rest of the chromosomes, but get pulled in later just before the newly forming nuclear membrane closes. "The DNA tether seems to keep the nuclear envelope from closing, and then the chromosome fragment just glides right in at the last moment," Sullivan said.

If this mechanism fails, however, and the chromosome fragment gets left outside the nucleus, the consequences are dire. The fragment forms a "micronucleus" with its own membrane and becomes prone to extensive rearrangements of its genetic material, which can then be reincorporated into chromosomes during the next cell division. Micronuclei and genetic rearrangements are commonly seen in cancer cells.

"We want to understand the mechanism that keeps that from happening," Sullivan said. "We are currently identifying the genes responsible for generating the DNA tether, which could be promising novel targets for the next generation of cancer therapies."

Sullivan has just received a new four-year, $1.5 million grant from the National Institute of General Medical Sciences to continue this research.

Graduate student Travis Karg is first author of the new paper, which shows that spindle microtubules play an important role in driving the delayed segregation of chromosome fragments. The other coauthors, in addition to Sullivan, are Mary Williard Elting and Sophie Dumont at UC San Francisco and Hannah Vicars at UC Santa Cruz. This work was supported by grants from the National Institutes of Health.

Article adapted from a University of California - Santa Cruz news release.

Publication: The chromokinesin Klp3a and microtubules facilitate acentric chromosome segregation. Travis Karg et al. Journal of Cell Biology (2017): Click here to view.

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'Hail Mary' Mechanism Can Rescue Cells with Severely Damaged Chromosomes, Researchers Say - Scicasts (press release) (blog)

June 5, 2017 In this dividing cell, chromosome fragments (red) remain in the middle of the green spindle structure, while the rest of the chromosomes have segregated to the two poles. Fragments that fail to segregate to daughter nuclei form micronuclei, resulting in an unstable genome and cancer. Credit: Travis Karg

The DNA vital to the life of a cell is packaged in chromosomes, and a variety of checkpoints, repair mechanisms, and other cellular safeguards exist to maintain the integrity of the chromosomes during cell growth and division. Those safeguards can fail, however, and a cell may find itself trying to divide into two daughter cells with a loose chromosomal fragment drifting away from a broken chromosome.

William Sullivan calls this a "worst case scenario" for the cell. The potential consequences include cell death or a cancerous cell growing out of control. But Sullivan, a professor of molecular, cell, and developmental biology at UC Santa Cruz, has found that the cell still has one more trick up its sleeve to rescue the broken chromosome.

The latest findings from Sullivan's lab, published in the June 5 issue of Journal of Cell Biology, reveal new aspects of a remarkable mechanism that carries broken chromosomes through the process of cell division so that they can be repaired and function normally in the daughter cells. Sullivan has been studying this process in the fruit fly Drosophila melanogaster. His lab has created a strain of flies in which broken chromosomes are common due to the expression of a DNA-cutting enzyme.

"We have flies in which 80 percent of the cells have double-strand breaks in the DNA, and the flies are fine," he said. "The cell has this amazing mechanism, like a Hail Mary pass with time running out."

The video will load shortly

The mechanism involves the creation of a DNA tether which acts as a lifeline to keep the broken fragment connected to the chromosome. Powerful new microscopy techniques enable researchers to observe the whole process in living cells, with bright fluorescent tags highlighting the chromosomes and other cellular components.

When a cell divides, it duplicates its chromosomes to make one set for each of the daughter cells. The membrane around the nucleus, which keeps the chromosomes separate from the rest of the cell, breaks down. The two sets of chromosomes then line up and segregate to opposite sides of the cell, pulled apart by a structure of microtubules called the spindle. A new nuclear envelope forms around each set of chromosomes, and new cell membranes separate the two daughter cells.

Sullivan's research has shown that chromosome fragments don't segregate with the rest of the chromosomes, but get pulled in later just before the newly forming nuclear membrane closes. "The DNA tether seems to keep the nuclear envelope from closing, and then the chromosome fragment just glides right in at the last moment," Sullivan said.

If this mechanism fails, however, and the chromosome fragment gets left outside the nucleus, the consequences are dire. The fragment forms a "micronucleus" with its own membrane and becomes prone to extensive rearrangements of its genetic material, which can then be reincorporated into chromosomes during the next cell division. Micronuclei and genetic rearrangements are commonly seen in cancer cells.

"We want to understand the mechanism that keeps that from happening," Sullivan said. "We are currently identifying the genes responsible for generating the DNA tether, which could be promising novel targets for the next generation of cancer therapies."

Sullivan has just received a new four-year, $1.5 million grant from the National Institute of General Medical Sciences to continue this research.

Graduate student Travis Karg is first author of the new paper, which shows that spindle microtubules play an important role in driving the delayed segregation of chromosome fragments. The other coauthors, in addition to Sullivan, are Mary Williard Elting and Sophie Dumont at UC San Francisco and Hannah Vicars at UC Santa Cruz. This work was supported by grants from the National Institutes of Health.

Explore further: Protective barrier inside chromosomes helps to keep cells healthy

More information: Travis Karg et al, The chromokinesin Klp3a and microtubules facilitate acentric chromosome segregation, The Journal of Cell Biology (2017). DOI: 10.1083/jcb.201604079

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'Hail Mary' mechanism can rescue cells with severely damaged chromosomes - Phys.Org

Queen's University Belfast Vice-Chancellor Patrick Johnston dies suddenly

BelfastTelegraph.co.uk

Queen's University Belfast's Vice-Chancellor Patrick Johnston has died suddenly.

http://www.belfasttelegraph.co.uk/news/northern-ireland/queens-university-belfast-vicechancellor-patrick-johnston-dies-suddenly-35787432.html

http://www.belfasttelegraph.co.uk/news/northern-ireland/article35787511.ece/af72b/AUTOCROP/h342/2016-09-19_new_24750948_I1.JPG

Queen's University Belfast's Vice-Chancellor Patrick Johnston has died suddenly.

The news of his death came in an email to staff from the university's registrar, James O'Kane on Sunday afternoon.

Professor Johnston's cause of death has not yet been revealed. Queen's University has said more information will be made available.

Obituary: Prof Patrick Johnston - a great mind whose work saved lives

In a statement the Queen's University said: "It is, with a deep sense of shock and loss, that I have to announce the untimely and sudden death of our Vice-Chancellor, Professor Patrick Johnston, earlier today.

"We extend our deepest sympathies and condolences to Iseult, his wife, and their four boys, Seamus, Eoghan, Niall and Ruairi, and the wider family circle at this desperately sad time.

"We will provide further updates in due course."

QUB academic and green party councillor John Barry said the news would come as a shock to staff at the Russell group university.

He said: "He was our first locally based Vice-Chancellor in quite some time - and was extremely youthful and energetic. It's a complete shock."

His loss will be felt not just at home here in Northern Ireland but right around the world where he was hugely respected. DUP leader Arlene Foster

The SDLP's Dr Alasdair McDonnell paid tribute to the "powerful figure" and said he was deeply saddened by news of Professor Johnston's death.

He said: "I am deeply saddened to hear the news of the untimely death of Professor Paddy Johnston. His death is a terrible loss to Queens University, cancer research and Northern Ireland.

Professor Johnston was a powerful figure, working to find a cure for cancer. One of his greatest achievements is undoubtedly leading the establishment of the Centre for Cancer Research and Cell Biology in Belfast.

I express my deepest sympathies and condolences to his family and QUB colleagues at this difficult time.

UUP MLA Alan Chambers said: "Many will remember Patrick particularly for his work in leading the establishment of the Centre for Cancer Research and Cell Biology.

"For his tireless work in this field we are indebted to him."

His loss will be keenly felt also by all those who admired his determination to find a cure for cancer and who respected his decision to return to Belfast to lead the Centre for Cancer Research. Sinn Fein MLA Mairtin O Muilleoir

Professor Johnston from Londonderry was the first person to be appointed President and Vice-Chancellor from within the staff of Queens since the appointment of Sir Peter Froggatt in 1976.

Professor Johnston was regarded as one of the world's leading cancer researchers.

He joined Queens University in 1996 as Professor of Oncology, later leading the establishment of the Centre for Cancer Research and Cell Biology.

Since then CCRCB has revolutionised cancer treatment in Northern Ireland and further afield. It now has 250 researchers from all over the world and was designated a Cancer Research UK Centre in 2009.

Until taking up the post of President and Vice-Chancellor of Queens in March 2014, Professor Johnston was Dean of the School of Medicine, Dentistry and Biomedical Sciences where he led the foundation of a new international Medical School and Institute of Health Sciences.

His own research focus over 25 years has been on the understanding of mechanisms of drug resistance to therapeutic agents.

This resulted in a number of prestigious landmark publications, more than 20 patents and the award of grants of 95m from research and philanthropic bodies including Cancer Research UK, the Medical Research Council, Atlantic Philanthropies, the Department of Health, Social Services and Public Safety and the National Institute of Health.

In 2012 he received a Diamond Jubilee Queens Anniversary Prize from Her Majesty The Queen for the University-led reorganisation of cancer care in Northern Ireland.

Belfast Telegraph Digital

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Queen's University Belfast Vice-Chancellor Patrick Johnston dies suddenly - Belfast Telegraph

June 2, 2017

As the cell's molecular control center, the mTor kinase regulates cellular metabolism, growth and division. However, in cells affected by pathological change, the regulation goes array. Therefore, it would be helpful if the central control could be simply turned off to suppress insulin resistance or cancerous growth for example. Scientists at the Leibniz-Forschungsinstitut fr Molekulare Pharmakologie (FMP) in Berlin (Germany) succeeded in locating a crucial off-switch for the central cell control. Paradoxically, this 'off-switch' is a lipid kinase producing a product previously known for its role in the activation of mTor. The results just appeared in the high-ranking journal 'Science'. They bolster the hopes of patients waiting for new effective therapies against diabetes, obesity, cancer and a rare congenital muscular disease.

The important control functions of the mTor kinase influence cell metabolism, division and growth. For example, the molecular control unit ensures the production of new proteins or the storage of fat and carbohydrates in metabolically active tissue. These processes are stimulated by the influx of sugar and amino acids and by signals initiated by growth factors including the insulin-like growth factor. If this influx does not occur in a starvation period, mTor switches the cell from anabolic to catabolic mode. Instead of synthesizing new proteins from amino acids, the cell now activates clean-up processes to remove damaged proteins, which could become hazardous for the cell or organ. The cleansing effect of interval fasting is attributed to the consequences of deactivating the mTor kinase.

In certain disease states, it would be sensible to shut down the mTor kinase complex. In cases of diabetes and obesity for example, pathological mutations exist in the cellular control center. This also applies to many cancers. This raises the question how and where to switch off such a complex mechanism.

A Surprising Discovery

To find this switch-off mechanism, researchers in the Leibniz-Forschungsinstitut fr Molekulare Pharmakologie (FMP) in Berlin kept a keen eye on nature's ways to accomplish this down regulation. According to known facts, the lysosomal mTor kinase complex becomes less active or inactive in extended hunger periods. The lysosome is the regular cell compartment for the mTor kinase complex activity. However, the complex also turns inactive several times during the day without leaving its membrane-bound place. This happens for example when the stimulating insulin signals do not arrive. Therefore, there has to be a natural mTor brake somewhere in this location. The discovery of this brake is now published in the top journal 'Science'. It came as a surprise even for FMP Director Professor Volker Haucke: "We found a local lipid kinase on the lysosome. This kinase deactivates mTor. Paradoxically, if the lipid product of this kinase is synthesized on the cell surface membrane, it is rather known as growth stimulating lipid, i.e. it has the exact opposite effect."

As the scientist discovered, another scarcely investigated specific class II lipid kinase (PI3KC2) exists in the cell, which deactivates the mTor complex on the lysosomal membrane in the absence of stimulating signals from the outside. In the absence of hormonal signals such as insulin or insulin-like growth factor (e.g. at night), the lipid kinase PI3KC2 becomes active at the lysosomal membrane. The active lysosomal lipid kinase phosphorylates a lipid, which then deactivates the mTor complex. Under these conditions the lysosome mainly functions to degrade cellular proteins.

The discovery of this off-switch for mTor sheds light on one of the riddles in basic cell biology. In addition, the new insights are of the highest relevance for clinical research projects. Doctoral candidate Alexander Wallroth in collaboration with Dr. Andrea Marat (a former postdoctoral researcher now working in New York) discovered the mTor brake. Alexander Wallroth comments: "We set out to discover biomedical applications, and our research is closing in on that goal."

Biomedical Applications are within Reach

The scientists set their immediate sights on practical applications in the treatment of obesity and diabetes. The well-known diabetes drug Metformin already utilizes the mTor repression by activating an enzyme in the same cascade as the now discovered lipid kinase.

Alexander Wallroth emphasizes: "If we succeed in activating the discovered lipid kinase, we will have another, possibly better shut-off switch for mTor. This will enable us to devise therapies, which influence sugar and fat metabolism. There is even a chance to influence the growth of malignant tumors. It is generally known that patients treated with Metformin are less prone to developing cancer even though obesity actually increases the cancer risk. Right now, our discovery may or may not be applicable to cancer therapies. However, our group considers new approaches within the range of the possible."

Now Underway: The Search for Active Agents

Scientists consider the lipid kinase PI3KC2 a particularly suitable therapeutic fulcrum because this kinase is not essential for survival. Targeted manipulations from outside the body would therefore be relatively safe. Therefore, scientists working in the screening unit of the FMP are busy hunting down activating and inhibiting substances, which are specific for the lipid kinase.

An activator could be useful for the treatment of diabetes and obesity because it will dampen mTor activity. An inhibitor could possibly be useful in other therapeutic applications: The lipid kinase now identified as an mTor inhibitor also plays a crucial role in myotubular myopathy. So far, there is no treatment for this disease, let alone a cure. Recently, Canadian scientists demonstrated in mouse and zebra fish models that switching off the lipid kinase PI3KC2 can at least partially cure a rare congenital myotubular myopathy (muscle weakness). So far however, the used inhibitors are unsuitable for use in humans because they also inhibit related enzymes. This alone is a good reason to search for a specific inhibitor.

While the FMP has not developed real drugs, the institute certainly can deliver the 'raw materials' for such development. In view of the started search for active drugs, Volker Haucke promises: "We discovered a new, potentially promising point to attack mTOR and are now pursuing possible therapeutic options. Following up on our work, there is a reasonable chance for our scientists to identify candidate molecules with the desired clinical effects someday."

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Scientists locate crucial off-switch for central cell control - News-Medical.net

June 1, 2017

Researchers have discovered important details of a vital process that enables cells to divide correctly into two.

Their findings shed light on the molecular processes that determine how and when key proteins combine, to help create a site required for accurate DNA separation over generations.

Researchers from the University of Edinburgh used biophysical and cell biology techniques to better understand the assembly of a key set of proteins known as Mis18.

Their study offers insights as to how the Mis18 protein complex controls the accumulation of another protein, known as CENP-A.

The CENP-A collects at a site where the dividing cell's DNA - which is packaged into a pair of chromosomes - connects and then divides into two cells.

By studying the molecular mass of the constituent Mis18 proteins as they combined, researchers were able to determine how many proteins of each type assembled to form a functional Mis18 complex.

They also found how a further protein, known as Cdk1, controls the timing of Mis18 assembly, by temporarily modifying one of the proteins involved to prevent it from binding the others.

The study, funded by the Wellcome Trust, was published in EMBO reports.

Dr Jeyaprakash Arulanandam, of the University of Edinburgh's School of Biological Sciences, who led the study, said: "These findings provide valuable insights into how cells help preserve the site essential for equal distribution of their DNA when they divide, and how the timing of this process is tied to the cell cycle."

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Passing skills down through the generations, previously thought to be unique to humanity, has been discovered in chimpanzees.

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Solving a 140-year old taxonomic puzzle, Cornell researchers have identified and described a new species of electric fish from the Ogoou River in Gabon, Africa.

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Key process for cell division revealed in molecular analysis - Phys.org - Phys.Org

Shreveport Times 1:06 p.m. CT June 1, 2017

Recent graduate Melissa Traver and current students Samantha Lyons and Andrianna Walsh won the top prize in the American Physiological Societys Video Contest.(Photo: Courtesy of Centenary College)

Recent Centenary College graduate Melissa Traver and current students Samantha Lyons and Andrianna Walsh have won the top prize in the American Physiological Societys Video Contest for their creative entry explaining the effects of this autoimmune syndrome on kidney function.

Lyons, Traver, and Walsh were all students in Dr. Cristina Caldaris Principles of Immunology course in fall 2016, and their video emerged from an assignment in the class. In the past, Caldari has used episodes of Mystery Diagnosis (a Discovery Life show) as a teaching tool in labs. The episodes feature patients who suffer from immune system issues, usually autoimmune disorders.

The end of the semester assignment is for groups of students to create their own Mystery Diagnosis video and present it to the rest of the class, explains Caldari. This past year I saw that the American Physiological Society had this video contest, so instead of creating a Mystery Diagnosis, I asked the students to prepare a video that would fit APSs criteria for the video contest and submit it to the competition.

The APS Function Follows Form video contest called for undergraduate and graduate students to create and submit short videos that explore a specific physiological function or system in a way that engages and educates the broader public.

Four groups of Caldaris students submitted videos to the contest this year, and Lyons, Traver, and Walsh took home the $750 top prize for Goodpasture syndrome and the kidneys, an illustrated description of kidney anatomy and physiology that also explores the effects of Goodpasture syndrome on kidney function. In patients with Goodpasture syndrome, antibodies created by the immune system attack the kidneys and sometimes also the lungs, leading to kidney dysfunction and eventual failure if left untreated.

The hardest part of the assignment was explaining complicated concepts with a very broad target audience in mind, explains Traver. We had to separate ourselves from what we had learned all semester and in other classes at Centenary to make complex ideas attainable for a general audience. We chose to do an illustrated video because we felt it was the most clear and concise way to explain the anatomy of the immune disorder.

Traver, who recently graduated summa cum laude and earned departmental honors in biology, is continuing her studies in a Ph.D. program in biochemistry and cell biology at Rice University.

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Centenary biology students win national video contest - Shreveport Times

University of Maryland researchers have found that a fairly common chemical may slow the aging process of human skin. The chemical, an antioxidant known as methylene blue, is completely safe and affordable. The research team found evidence that this chemical may also even completely reverse the most common signs of aging. They tested cultured skin cells along with simulated skin tissue. It is possible this chemical will eventually be used as an antioxidant in a number of different skin care products. The study was led by senior author Kan Cao. He is an associate professor of molecular genetics and cell biology at the University of Maryland. The details of the study were recently published online in the journal Scientific Reports.

About the Study

The research team tested methylene blue for nearly an entire month in skin cells taken from healthy donors. These individuals were middle-aged. Skin cells from those who suffer from progeria were also tested. Progeria is a genetic disease that copies theaging process at a heightened rate. The research team tested three additional antioxidants in addition to methylene blue: MitoTEMPO (mTEM), MitoQ and N-Acetyl-L-Cysteine.

Methylene blue outperformed the other antioxidants in the experiments. It boosted numerous age-related cell symptoms in progeria patients as well as the healthy donors. The skin cells exhibited a reduction in harmful molecules called "reactive oxygen species, a decrease in cell death rates and a bump in cell division rates across the four-week treatment period.

Cao's research team also tested methylene blue in skin cells from older individuals. These donors were 80 years-old or older. Their skin cells were tested for a four-week period. Once treatment culminated, the cells from the comparably old donors endured a wide array of improvements like thediminished expression of two genes (senescence-associated p16 and beta-galactosidase)used to indicate cell aging.

A Closer Look at the Results

Cao reports the effects of methylene blue are not temporary. This chemical produces long-lasting and fundamental alterations to skin cells for skin of all ages. The study's lead author, Zheng-Mei Xiong, states he was excited to see skin cells taken from individuals beyond 80 years of age grow far better in the medium containing methylene blue with lower cell senescence markers. Xiong is an assistant research professor of molecular genetics and cell biology at the University of Maryland.

About the Simulated Human Skin Used in the Experiments

The research team used simulated human skin to conduct even more tests. The simulated skin is a 3D model comprised of living skin cells. It is made of all the primary structures and layers of skin tissue but for sweat glands and hair follicles. This model skin is also usable in skin irritation tests mandated by the Food and Drug Administration in order to approve cosmetic products that are poised to hit the market.

The simulated skin empowered the research group to test all sorts of different aging symptoms that could not be replicated within cultured cells. It is interesting to note the simulated skin treated with methylene blue held onto more water and became thicker. Both of these characteristics are typical of youthful skin. The simulated skin was also used to gauge the safety of cosmetic ointments with added methylene blue. The results indicate methylene blue spurs minimalirritation even at especially high concentrations.

What's Next

Cao and Xiong are working on ways for people to enjoy the benefits of methylene blue's unique properties. The research team has already started the formulation of cosmetics with this chemical. They hope to bring products to the market inthe near future.

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Antioxidant Could Slow Skin Aging - Anti Aging News

Cosmetic products have offered the promise of younger and more youthful looking skin for centuries, yet few, if any, deliver on such a promise. However now, new data from a team of University of Maryland investigators suggests that the thiazine dye methylene blue, which has been used medicinally, may also slow the aging of human skin. Findings from the new study were published recently in Scientific Reports in an article entitled Anti-Aging Potentials of Methylene Blue for Human Skin Longevity.

The UMD team tested the methylene blue for 4 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).

"Our work suggests that methylene blue could be a powerful antioxidant for use in skin care products," explained senior study investigator Kan Cao, Ph.D., 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."

In the current study, methylene blue outperformed the other three antioxidants, improving several age-related symptoms in cells from both healthy donors and progeria patients. The skin cellsfibroblasts that produce the structural protein collagenexperienced a decrease in damaging molecules known as reactive oxygen species (ROS), a reduced rate of cell death, and an increase in the rate of cell division throughout the 4-week treatment.

Interestingly, the researchers also tested methylene blue in fibroblasts from older donors (>80 years old) for a period of 4 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 -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," noted lead study investigator Zheng-Mei Xiong, Ph.D., assistant research professor of cell biology and molecular genetics at UMD. "Methylene blue demonstrates a great potential to delay skin aging for all ages."

To take their results one step further, the UMD team used the simulated human skin to perform several more experiments. This simulated skina 3D model made of living skin cellsincludes all the major layers and structures of skin tissue, with the exception of hair follicles and sweat glands.

"This system allowed us to test a range of aging symptoms that we can't replicate in cultured cells alone," Dr. Cao noted. "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."

Additionally, the investigators used the model skin to test the safety of cosmetic creams with methylene blue added. The results suggested that methylene blue causes little to no irritation, even at high concentrations. Encouraged by these results, the research team hopes 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," Dr. Cao concluded. "We are also very excited to develop this 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."

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Dyeing Your Way to Younger Skin? - Genetic Engineering & Biotechnology News

Rising popularity of kinetic research over fixed cellular analysis is the key driver.

Addition of dyes and reagents alter the cell behavior, mostly in a negative manner, which does not showcase the natural course of action of the cellular functions.

Understanding the cellular behavior in its natural state is crucial in drug discovery and targeted drug therapy.

In a survey by Drug Discovery World Spring, almost 21% researchers prefer & use live cell imaging and 31% plan to use it in the future. Moreover, 38% of the respondents were interested in using live cell kinetic HCS imaging in the future. The most important feature for researchers is the ability to automate the incubation and image capturing of any live cell analyzer.

Equipment dominated the product segment in 2016. The current system, although of great potential are still expected to perform better over the next few years. The general trend is to make the instruments compact and integrated for end-to-end processing.

Cell biology dominated the application with more than 30% of the shares and was closely followed by developmental biology. Stem cell and drug discovery are the upcoming fields to apply live cell imaging in the research.

The global live cell imaging market is expected to reach USD 9.3 billion by 2025, according to a new report by Grand View Research, Inc.

Rising popularity of kinetic research over fixed cellular analysis is the key driver. Addition of dyes and reagents alter the cell behavior, mostly in a negative manner, which does not showcase the natural course of action of the cellular functions. Understanding the cellular behavior in its natural state is crucial in drug discovery and targeted drug therapy. This, in turn, increases the need for live cell imaging, thus boosting the market.

In a survey by Drug Discovery World Spring, almost 21% researchers prefer & use live cell imaging and 31% plan to use it in the future. Moreover, 38% of the respondents were interested in using live cell kinetic HCS imaging in the future. The most important feature for researchers is the ability to automate the incubation and image capturing of any live cell analyzer. Secondly, they also give importance to viable cell-tracking ability of the equipment. Further development in the technology of equipment is expected to fulfill these criteria and boost the utility of the same over the forecast period.

Development in delivering probes in living cells, targeting organelles, and proteins using some of the techniques has increased use and adoption of live cell imaging in research and other applications. With improved fluorescent probes, the techniques such as Fluorescence Resonance Energy Transfer (FRET) share a majority of the share.

Further Key Findings From The Report Suggest: Equipment dominated the product segment in 2016. The current system, although of great potential are still expected to perform better over the next few years. The general trend is to make the instruments compact and integrated for end-to-end processing.

Cell biology dominated the application with more than 30% of the shares and was closely followed by developmental biology. Stem cell and drug discovery are the upcoming fields to apply live cell imaging in the research.

North America dominated due to its high investment rate and technologically sound infrastructure. The research firms present in this region are technologically aware, hence, readily invest in high cost equipment.

Asia Pacific is expected to show fastest growth over the forecast period due to increasing application of these imaging techniques in drug discovery and personalized medicine.

Read the full report: http://www.reportlinker.com/p04899210/Live-Cell-Imaging-Market-Analysis-By-Product-Application-Technology-Time-lapse-Microscopy-Fluorescence-Recovery-After-Photobleaching-Fluorescence-Resonance-Energy-Transfer-High-Content-Screening-Segment-Forecasts.html

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Live Cell Imaging Market is expected to reach USD 9.3 billion by 2025 - PR Newswire (press release)