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duminică, 5 august 2012

Molecule Discovered That Converts Stem Cells Into Heart Cells

For years, scientists have been looking for a good source of heart cells that can be used to study cardiac function in the lab, or perhaps even to replace diseased or damaged tissue in heart disease patients. To do this, many are looking to stem cells. Researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham), the Human BioMolecular Research Institute, and ChemRegen, Inc. have been searching for molecules that convert stem cells to heart cells for about eight years - and now they've found one. Writing in Cell Stem Cell, the team describes how they sifted through a large collection of drug-like chemicals and uncovered ITD-1, a molecule that can be used to generate unlimited numbers of new heart cells from stem cells.

"Heart disease is the leading cause of death in this country. Because we can't replace lost cardiac muscle, the condition irreversibly leads to a decline in heart function and ultimately death. The only way to effectively replace lost heart muscle cells - called cardiomyocytes - is to transplant the entire heart," said Mark Mercola, Ph.D., director of Sanford-Burnham's Muscle Development and Regeneration Program and senior author of the study. "Using a drug to create new heart muscle from stem cells would be far more appealing than heart transplantation."

Searching for a needle in a haystack

Stem cells are important because they do two unique things - 1) self-renew, producing more stem cells and 2) differentiate, becoming other, more specialized cell types. To obtain a large number of a certain cell type, such as heart cells, the hard part is figuring out the signals that direct them to become the desired cell type.

Mercola's group has been hunting for heart-inducing signals for 15 years - in embryos and in stem cells. To find a synthetic molecule that might one day lead to a drug therapy to regenerate the heart, they joined forces with a team of medicinal chemists at the Human BioMolecular Research Institute led by John Cashman, Ph.D. With funding from the California Institute for Regenerative Medicine, they used sophisticated robotic technology to methodically test a large collection of drug-like chemicals, looking for that needle in a haystack that, when added to stem cells, results in cardiomyocytes. The winning compound was ITD-1.

Therapeutic applications

There's no shortage of therapeutic possibilities for ITD-1. "This particular molecule could be useful to enhance stem cell differentiation in a damaged heart," explained Erik Willems, Ph.D., postdoctoral researcher in Mercola's lab and first author of the study. "At some point, it could become the basis for a new therapeutic drug for cardiovascular disease - one that would likely limit scar spreading in heart failure and promote new muscle formation."

Mercola, Willems, and Cashman are now working with San Diego biotech company ChemRegen, Inc. to further develop ITD-1 into a drug that one day might be used to treat patients.

More scientific detail

The researchers discovered that ITD-1 blocks a cellular process known as TGF? signaling. TGF? (short for transforming growth factor-?) is a protein produced by one cell type to influence others' behaviors, such as proliferation, scarring, and even stem cell differentiation. TGF? works from outside the cell, binding to a receptor on the surface of a responding cell to initiate an intracellular signaling cascade that causes genes to be switched on or off, ultimately altering cellular behavior - in this case making heart muscle.

ITD-1 triggers degradation of the TGF? receptor, thus inhibiting the whole process. With TGF? signaling turned off, stem cells are set on a course toward cardiogenesis. ITD-1 is the first selective inhibitor of TGF?, meaning that it might also have applications in many other processes controlled by TGF?.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our heart disease section for the latest news on this subject. This research was funded by the California Institute for Regenerative Medicine, the National Heart, Lung, and Blood Institute of the U.S. National Institutes of Health, the Human BioMolecular Research Institute, the American Heart Association, the German Research Foundation, and the T Foundation.
The study was co-authored by Erik Willems, Sanford-Burnham and ChemRegen Inc.; Paul J Bushway and Joaquim Cabral-Teixeira, Sanford-Burnham; Dennis Schade, ChemRegen Inc. and Human BioMolecular Research Institute; Wenqing Cai, Sanford-Burnham; Patrick Reeves, Harvard Medical School; Marion Lanier, ChemRegen Inc. and Human BioMolecular Research Institute; Christopher Walsh, Salk Institute for Biological Studies; Tomas Kirchhausen, Harvard Medical School; Juan Carlos Izpisua Belmonte, Salk Institute for Biological Studies and Center for Regenerative Medicine in Barcelona; John Cashman, ChemRegen Inc. and Human BioMolecular Research Institute; Mark Mercola, Sanford-Burnham and ChemRegen Inc.
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Critical Molecular Switch Discovered That Regulates Autophagy

The body has a built-in system known as autophagy, or 'self-eating,' that controls how cells live or die. Deregulation of autophagy is linked to the development of human diseases, including neural degeneration and cancer.

In a study published online this week in the Proceedings of the National Academy of Sciences, scientists at the Ludwig Institute for Cancer Research in Oxford discovered a critical molecular switch that regulates autophagy. They also studied the links between autophagy and a cellular process called senescence that stops cell growth permanently.

The researchers identified ASPP2, a tumor suppressor, as a molecular switch that can dictate the ability of a common cancer gene, known as the RAS oncogene, to either stop or promote senescence.

As Yihua Wang and researchers in Xin Lu's group at the Ludwig Institute investigated the life cycle of fibroblast cells - the most common connective tissue cells in animals - they found that reduced levels of the ASPP2 protein increase RAS oncogene-induced autophagic activity. This in turn prevented cells from entering senescence. Without ASPP2, the cells continued to proliferate unchecked, thereby promoting tumor growth.

ASPP2 is known to play a role in suppressing tumor development. Mice that have a deficiency or malfunction in this protein have a predisposition to developing tumors. And low ASPP2 levels in patients are linked to poor prognoses in cancers, such as large B-cell lymphomas. Reduced ASPP2 expression has also been observed in highly metastatic breast tumors. But until now, researchers did not understand why.

"We found that in the presence of the common cancer-causing RAS oncogene, ASPP2 interacted with a protein complex that is responsible for deciding cell fate via autophagy," said Yihua Wang, PhD, Ludwig researcher in Oxford.

"What this means is that the cell's emergency stop button is disabled when ASPP2 expression is reduced or lost, allowing it to proliferate unchecked as with cancer," added Wang.

"The balance between the RAS oncogene and ASPP2 activity is crucial to determining whether or not tumor growth is promoted. Our next step will be to identify ways to alter ASPP2 activity at that critical switch point. This could be an effective way to treat cancers with reduced ASPP2 expression and mutated RAS, such as breast and colon cancers," concluded Wang.

"Some of the recently developed anti-cancer drugs are potent inducers of autophagy. The new findings may also offer an explanation as to why patient response to these drugs can vary dramatically. There are factors at play within the body that can dictate authophagic activity and impact clinical outcomes," said Xin Lu, PhD, director of Ludwig's Oxford Branch. "While further study is needed, these findings may in the longer term help doctors to identify patients who are more likely to respond well to autophagic inhibition," added Lu.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Genetic Clue Discovered For Why Women Outlive Men

A new study of mitochondrial DNA in fruit flies offers a number of clues that might explain why females tend to outlive males across much of the animal kingdom, including humans.

Researchers from Monash University in Australia and Lancaster University in the UK, write about their work in the 2 August online issue of Current Biology.

They found male fruit flies appear to have mutations in their mitochondrial DNA that affect how fast they age and how long they live.

Scientists use fruit flies as models for studies in genes and aging because their biological processes are remarkably similar to that of other animals, such as humans, and with a lifespan of about a month, it doesn't take too long to investigate generational effects.

Senior author Damian Dowling, a research fellow in the Monash School of Biological Sciences, told the press:

"All animals possess mitochondria, and the tendency for females to outlive males is common to many different species. Our results therefore suggest that the mitochondrial mutations we have uncovered will generally cause faster male aging across the animal kingdom."

"Intriguingly, these same mutations have no effects on patterns of aging in females. They only affect males," he added.

Mitochondria are special subunits of cells, about the same size as bacteria, that provide the energy for life. They combine sugar and oxygen into adenosine triphosphate or ATP, molecular packets of energy that are usable by cells.

Mitochondria have their own DNA that is quite separate from the cellular DNA in the nucleus of the cell.

And, unlike cellular DNA, which is inherited from the sperm and egg that fuse to make the new individual, mitochondrial DNA comes only from the egg.

Thus, as mitochondrial DNA is passed down from generation to generation, the process of natural selection has no opportunity to "screen out" mutations in mitochondrial DNA that might be harmful to males. The researchers refer to this as a "sex-specific selective sieve".

For their study, Dowling and colleagues looked at differences in longevity and biological aging in male and female fruit flies whose mitochondria came from different origins.

They found genetic variations in both male and female mitochondrial DNA, but only the male ones could be linked to life expectancy. There weren't just a few mutations in one place, there were several, spread all over the mitochondrial genome:

"... our results indicate that the mitochondrial mutation loads affecting male aging generally comprise numerous mutations over multiple sites," they write.

The researchers suggest the mutations are entirely due to the way mitochondrial DNA is passed down through the female line.

"If a mitochondrial mutation occurs that harms fathers, but has no effect on mothers, this mutation will slip through the gaze of natural selection, unnoticed. Over thousands of generations, many such mutations have accumulated that harm only males, while leaving females unscathed," Dowling explained.

In an earlier study that looked at the effect of mitochondria being passed down the female line, the team had also discovered a link with male infertility.

Dowling said combining this latest study with their earlier work suggests mitochondria are "hotspots" for mutations that influece male health.

"What we seek to do now is investigate the genetic mechanisms that males might arm themselves with to nullify the effects of these harmful mutations and remain healthy," said Dowling.

Written by Catharine Paddock PhD
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our seniors / aging section for the latest news on this subject. "Mitochondria, Maternal Inheritance, and Male Aging "; M. Florencia Camus, David J. Clancy, Damian K. Dowling; Current Biology, 02 August 2012; DOI: 10.1016/j.cub.2012.07.018; Link to Abstract.
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posted by Ecologist on 4 Aug 2012 at 5:27 am
The idea is that males get mitochondria only from their mother, but the problem with it is that both males and females inherit mitochondria from their mother. This is not a nuclear scene where there are two sets of genes (or alleles), and the defect goes unnoticed in a female. At most this is a one-generation effect between the mother and her sons. There is also a one-generation effect between the mother and her daughters. Unless the researcher is proposing that male cells interact with their mitochondria in ways that females do not, then there is a logic flaw in their argument.
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posted by Kitfox on 3 Aug 2012 at 6:56 am
Is this research screening all flies or just the married ones? The data could be flawed. What we need to look into is the nagging genes of the females of the species and turn it off. Once that has been achieved the males will no longer mutate their genes ON PURPOSE in order to shorten the suffering period. :)
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'Genetic Clue Discovered For Why Women Outlive Men'
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marți, 13 decembrie 2011

Method To Produce Proteins In Laboratory Has Now Been Discovered

Main Category: Biology / Biochemistry
Article Date: 13 Dec 2011 - 1:00 PST

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The most abundant and important molecules in all living organisms are proteins; after all they manage to participate in every single one of life's essential reactions. So it is easy to see why scientists have been making such a fuss trying to learn how to synthesise them in laboratory as this would provide them with a tool of extraordinary potential. Unfortunately, this has not proved easy. But an article just out in the journal Science by Bruno Correia, Mihai Azoitei, William Schief and colleagues from the Biochemistry Department of Washington University and the Institute Gulbenkian of Science in Portugal might have found a solution.

The study describes a new method, which the researchers show to work by synthesising a totally new protein that they think can help in the development of a highly effective vaccine against HIV. This result proves the potential of a protocol that, like Correia points out "can now be used to design any protein whether to treat disease, create food, new sources of energy and even for totally new, not yet imagined, functions".

Synthesis of Proteins in Laboratory - one of the "holy grails" of molecular biology, much talked, much chased but not really achieved. The problem is that the function of a protein is determined by its three-dimensional (3D) structure, which in turn is the result on the physicochemical interactions of its different aminoacids (the "bricks" that form the protein). And to predict the combination of amino acids that will give origin to the 3D structure that have the function we want has proved, so far, too difficult.

The new approach by Correia and Azoitei tries to overcome the problem by using a combination of two well known methods - the so called evolutional protocol, in which proteins with a function similar to the one we want are mutated in an attempt to "evolve" into the desired protein and computational design where computers, departing from the different amino acids' characteristics, attempt to predict their right combination to generate the 3D structure with the function we want. In fact,alone, each of these methods has proven to have impossible limitations for example, in the first case, the number of mutated proteins to test is just too large as even a (small) protein of just 100 amino acids will have more than 20 to the power of 100 different mutations (and there is no guarantee that at least one will be functional). In the second method, the problem resides in our still limited lack of computational power that make accurate predictions except for a few very simple proteins impossible . "Our strategy, on the other hand, works explains Correia because we take the best of each of the 2 methods, using the capacity of the computation programs to explore an enormous space of sequences, and the efficiency of the evolutional method to select those that perform the desired function. "

To test the effectiveness of the new strategy the researchers next tried to create a protein that could serve as basis for a more effective vaccine against HIV then the ones developed so far.

So vaccines work by injecting a dead, attenuated or partial pathogen into the organism we want to protect against the pathogen. This triggers an immune response (without disease) that leaves an "immune memory", that if the organism is one day confronted with the "real thing" , rapidly sets off a fast and powerful immune defence. Anti-viral vaccines have a problem though and this is the reason why there are so few and also why we need a new flu vaccine every year and that is that viruses mutate/change rapidly making "immune memories" too often quickly irrelevant. To overcome the problem Correia and Azoitei used the new method to create a totally new protein, one that contained essential "bits" of HIV , essential in the sense that they are known to never mutate. In this case were used parts of the gp120 protein, the molecule used by the virus to get inside the cells to infect.

So how exactly does the new method works?

To start computational methods are used to find the best protein to transplant the gp120 "bits" into (so a protein with a shape that would not disrupt their 3D structure) and then the resulting molecule is mutated (to make it "evolve"). The proteins obtained (each with a different mutation) are then analysed, again by computers, to find the one with a 3D structure closer to HIV. This assures that the antibodies against the vaccine would be highly effective against the live virus.

"And although we are at early stages concludes Correia we hope that our protein can be used to develop a more effective vaccine against HIV as is one that is not expected to lose "power" (memory) over time. And since the method seems to work the possibilities now are endless, after all from diabetes to haemophilia, to mad cow disease and even cancer or Alzheimer's, the problem is always the same: a defective or absent protein..."

Article adapted by Medical News Today from original press release. Source: Ciência Viva
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joi, 8 decembrie 2011

Likely Cause Of Essential Tremor Discovered

Main Category: Neurology / Neuroscience
Article Date: 08 Dec 2011 - 1:00 PST

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Researchers from the CHUQ research center and Universite Laval have discovered the likely cause of essential tremor (ET), a neurological disorder that affects more than 10 million North Americans. The team's promising findings were published in a recent edition of the scientific journal Brain.

Frequently confused with Parkinson's disease, ET is the most common involuntary movement disorder. An estimated 4% of the population over 40 is affected by this neurological condition which manifests as muscle tremors, normally in the face, neck, and vocal chords.

The research team noticed a decrease in the concentration of GABA receptors in the cerebellum of patients suffering from ET. GABA receptors relay "chemical messages" which transmit inhibitory information to the different parts of the brain and play an essential role in the human body. A loss of GABA receptors in the cerebellum could affect the function of the cerebellum, an organ beneath the brain that manages communication between the brain and muscles and coordinating movements.

"This is one of the first demonstrations of biochemical changes in the cerebellum in patients with ET. It's a real step forward that opens the doors to new avenues of research, and perhaps to new treatments down the road. It's possible that stimulating GABA receptors could help patients control, or even reduce, essential tremor," said Dr. Frédéric Calon, researcher at the CHUQ research center and professor at Université Laval's Faculty of Pharmacy. "This is one of the first times such large sample groups have been used to study ET," he continued.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our neurology / neuroscience section for the latest news on this subject. In addition to Dr. Calon, study authors were Sarah Paris-Robidas, Élodie Brochu, Marion Sintes, Vincent Emond, Mélanie Bousquet, Milène Vandal, Mireille Pilote, Cyntia Tremblay, and Thérèse Di Paolo from the CHUQ research center and Université Laval's Faculty of Pharmacy, as well as Ali H. Rajput and Alex Rajput from the University of Saskatchewan.
The research was made possible by a grant from the International Essential Tremor Foundation.
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