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orasa sukmark

Shot of Young Stem Cells Makes Rapidly Aging Mice Live Much Longer and Healthier - Gate... - 1 views

  • animals that got the stem/progenitor cells improved their health and lived two to three times longer than expected,
  • "Our experiments showed that mice that have progeria, a disorder of premature aging, were healthier and lived longer after an injection of stem cells from young, healthy animals," Dr. Niedernhofer said. "That tells us that stem cell dysfunction is a cause of the changes we see with aging."
  • "Typically the progeria mice die at around 21 to 28 days of age, but the treated animals lived far longer -- some even lived beyond 66 days. They also were in better general health."
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  • we injected stem/progenitor cells from young, healthy mice into the abdomens of 17-day-old progeria mice,
  • As the progeria mice age, they lose muscle mass in their hind limbs, hunch over, tremble, and move slowly and awkwardly. Affected mice that got a shot of stem cells just before showing the first signs of aging were more like normal mice, and they grew almost as large.
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    the experiment from the University of Pittsburgh shows that the mice can be stronger live longer after they were injected with stem cells from young healthy animals.
Nitchakan Chaiprukmalakan

How a single gene mutation leads to uncontrolled obesity - 0 views

  • Researchers at Georgetown University Medical Center have revealed how a mutation in a single gene is responsible for the inability of neurons to effectively pass along appetite suppressing signals from the body to the right place in the brain.
  • The research team specifically found that a mutation in the brain-derived neurotrophic factor (Bdnf) gene in mice does not allow brain neurons to effectively pass leptin and insulin chemical signals through the brain. In humans, these hormones, which are released in the body after a person eats, are designed to "tell" the body to stop eating. But if the signals fail to reach correct locations in the hypothalamus, the area in the brain that signals satiety, eating continues.
  • He has found that the gene produces a growth factor that controls communication between neurons.
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  • The Bdnf gene generates one short transcript and one long transcript. He discovered that when the long-form Bdnf transcript is absent, the growth factor BDNF is only synthesized in the cell body of a neuron but not in its dendrites. The neuron then produces too many immature synapses, resulting in deficits in learning and memory in mice. Xu also found that the mice with the same Bdnf mutation grew to be severely obese
  • large-scale genome-wide association studies showed Bdnf gene variants are, in fact, linked to obesity.
  • both leptin and insulin stimulate synthesis of BDNF in neuronal dendrites in order to move their chemical message from one neuron to another through synapses. The intent is to keep the leptin and insulin chemical signals moving along the neuronal highway to the correct brain locations, where the hormones will turn on a program that suppresses appetite.
  • "If there is a problem with the Bdnf gene, neurons can't talk to each other, and the leptin and insulin signals are ineffective, and appetite is not modified
  • One possible strategy would be to produce additional long-form Bdnf transcript using adeno-associated virus-based gene therapy, Xu says. But although this kind of gene therapy has proven to be safe, it is difficult to deliver across the brain blood barrier,
Nitchakan Chaiprukmalakan

Missing Lincs - Science News - 6 views

    • Nitchakan Chaiprukmalakan
       
      Scientists are finding more information about the importance of the non coding RNAs, lincRNAs.
  • Only now have scientists begun identifying the previously invisible contractors who make sure that materials get where they are supposed to be and in the right order to build a human being or any other creature. Some of these little-known workers belong to a class of molecules called long intergenic noncoding RNAs.
  • And the lincRNAs originate in what scientists used to view as barren wastelands between protein-coding genes. But new research is showing that these formerly underappreciated workers have important roles in projects both large and microscopic.
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  • In the last few years, scientists have learned that lincRNAs, as well as other RNAs that are long and noncoding but not intergenic, perform a variety of jobs. Some serve as guides showing proteins where to go, while others tether proteins to different types of RNA, or to DNA. Some work as decoys, distracting regulatory molecules from their usual assignments. Some may even have multiple roles, all the while chattering away to other RNA within cells. (It is not idle gossip; RNA communication within cells may ward off diseases such as cancer.) And as the ultimate multitaskers, lincRNAs keep proper cellular development ticking along and help define what makes mice mice and people people.
  • That archive contains about 3 billion genetic letters, far more than the genomes of less complex organisms such as roundworms and fruit flies.
  • In 2005, the research revealed that even though genes that code for proteins make up only 1.5 percent of the mouse genome, more than 63 percent of the genome’s DNA is copied into RNA. In humans the number is even higher, with up to 93 percent of the genome made into RNA, even though protein-coding genes make up less than 2 percent of the genome.
  • At first, many scientists didn’t know what to make of the excess RNA. Some thought it was overexuberance on the part of the DNA-copying machinery. But gradually researchers began to realize that many of those extra RNAs had important jobs to do.
  • Some, though, appear to act like general contractors — not hammering in the nails and pouring the foundations of cells themselves, but dictating how the job should be done.
  • One of the most famous long noncoding RNAs, known as XIST, is also one of the most hands-on. XIST is in charge of shutting down one of the X chromosomes in every single cell of women and girls
  • XIST doesn’t have a long commute to work; it coats whichever X chromosome makes it, preventing other genes on the chromosome from being activated
  • One of the most well-studied linc­RNAs, named HOTAIR, wasn’t lucky enough to get a job close to home. It is copied from DNA on chromosome 12 but has to travel to chromosome 2 to shut down several genes in a group known as the HOXD cluster, genes important for proper development of an organism
  • Not only does HOTAIR help direct development, but it is also important throughout life to help cells pinpoint their location in the body.
  • Whether promoting health or mis­directing cells, lincRNAs don’t necessarily act alone.
  • A lincRNA known as HOTTIP also works with a crew of histone modifiers, but instead of shuttering genes, HOTTIP’s crews hang grand-opening signs to attract gene-activating machinery
  • In the recipe for humans, lincRNAs are in the thick of things from the very beginning. At least 26 different lincRNAs need to be on to keep an embryonic stem cell a stem cell
  • Just how lincRNAs choose which genes to turn on and off isn’t yet known. But Pier Paolo Pandolfi, a geneticist at Beth Israel Deaconess and Harvard Medical School, suspects that the lincRNAs are whispering to each other and to other RNAs, keeping tabs on all a cell’s goings-on. Pandolfi laid out his hypothesis for how this chatter might help control protein production and other processes in the Aug. 5 Cell.
  • The Columbia team and Pandolfi’s team independently found that tweaking levels of a few messenger RNAs that distract microRNAs from PTEN messenger RNA can lead to prostate cancer or a type of brain tumor called glioblastoma. Just messing with levels of a messenger RNA from another gene known as ZEB2 throws off PTEN protein levels and can lead to melanoma in mice, Pandolfi’s group reported in another paper in the Oct. 14 Cell.
  • Losing one noncoding RNA may be disastrous for a cell, but for want of noncoding RNAs whole species may never have evolved, argues Queensland’s Mattick. He and others say the real function of lincRNAs is to give evolution a sort of molecular clay from which to mold new designs.
  • Humans have several lincRNAs that are found in no other species. Many of those RNAs are made in the brain, leading scientists to speculate that the molecules may be at least partially responsible for that important organ’s evolution.
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    Is RNA the most important molecule in the cell? There is a lot of evidence leading to new understandings of RNA and it's role in many different mechanisms within a cell.
nidthamsirisup

Engineered stem cells seek out and kill HIV in living mice - 0 views

  • human stem cells can be genetically engineered into HIV-fighting cells
  • surrogate model
  • CD8 cytotoxic T lymphocytes -- the "killer" T cells that help fight infection -- from an HIV-infected individual and identified the molecule known as the T cell receptor, which guides the T cell in recognizing and killing HIV-infected cells.
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  • cloned the receptor and used this to genetically engineer human blood stem cells.
  • mature T cells that can attack HIV in tissues where the virus resides and replicates.
  • CD4 cells are white blood cells that are an important component of the immune system, helping to fight off infections.
  • CD4 "helper" T cells
  • engineering stem cells to form immune cells that target HIV is effective in suppressing the virus in living tissues in an animal model
  • increased
  • HIV in the blood decreased.
    • wasin kusakabe
       
      Using mice as lab rats, researchers are able to produce a large amount of T cells that can fight off HIV more effectively.
  • The engineered stem cells developed into a large population of mature, multi-functional HIV-specific CD8 cells that could specifically target cells containing HIV proteins. The researchers also discovered that HIV-specific T cell receptors have to be matched to an individual in much the same way an organ is matched to a transplant patient.
  • Expanding on previous research providing proof-of-principle that human stem cells can be genetically engineered into HIV-fighting cells
  • In this current study, the researchers similarly engineered human blood stem cells and found that they can form mature T cells that can attack HIV in tissues where the virus resides and replicates. They did so by using a surrogate model, the humanized mouse, in which HIV infection closely resembles the disease and its progression in humans.
  • increased, while levels of HIV in the blood decreased. CD4 cells are white blood cells that are an important component of the immune system, helping to fight off infections. These results indicated that the engineered cells were capable of developing and migrating to the organs to fight infection there.
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    Stem cells that are engineered to produce T cells that can help fight off HIV.
nidthamsirisup

Stem Cell Treatment Spurs Cartilage Growth - Science News - 0 views

  • A small molecule dubbed kartogenin encourages stem cells to take on the characteristics of cells that make cartilage, a new study shows
  • And treatment with kartogenin allowed many mice with arthritis-like cartilage damage in a knee to regain the ability to use the joint without pain.
  • Kartogenin steers the stem cells to wake up and take on cartilage-making duties. This is an essential step in the cartilage repair that falls behind in people with osteoarthritis, the most common kind of arthritis, which develops from injury or long-term joint use.
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  • The molecule turned on genes that make cartilage components called aggrecan and type II collagen. Tests of mice with cartilage damage similar to osteoarthritis showed that kartogenin injections lowered levels of a protein called cartilage oligomeric matrix protein. People with osteoarthritis have an excess of the protein, which is considered a marker of disease severity.
  • kartogenin inhibits a protein called filamin A in the mesenchymal stem cells
chanon chiarnpattanodom

A new class of obesity genes encodes leukocyte adhesion receptors - 0 views

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    Obesity is controlled by a number of factors, mainly 2 factors genetics and the environment. Here they use 2 groups + 1 control group mice to compare obesity.
nidthamsirisup

Epigenetics: DNA Isn't Everything - 0 views

  • Research into epigenetics has shown that environmental factors affect characteristics of organisms. These changes are sometimes passed on to the offspring.
  • A certain laboratory strain of the fruit fly Drosophila melanogaster has white eyes. If the surrounding temperature of the embryos, which are normally nurtured at 25 degrees Celsius, is briefly raised to 37 degrees Celsius, the flies later hatch with red eyes.
  • crossed the flies for six generations. In this experiment, they were able to prove that the temperature treatment changes the eye colour of this specific strain of fly, and that the treated individual flies pass on the change to their offspring over several generations. However, the DNA sequence for the gene responsible for eye colour was proven to remain the same for white-eyed parents and red-eyed offspring.
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  • Epigenetics examines the inheritance of characteristics that are not set out in the DNA sequence.
  • important factors are the histones, a kind of packaging material for the DNA, in order to store DNA in an ordered and space-saving way. It is now clear that these proteins have additional roles to play. Depending on the chemical group they carry, if they are acetylated or methylated, they permanently activate or deactivate genes.
  • New methods now allow researchers to sometimes directly show which genes have been activated or deactivated by the histones
  • The genetic information of the DNA is passed on along with the relevant epigenetic information for the respective cell type.
  • A similar question remains for the inheritance of the epigenetic characteristics from parents to offspring. They now know that when the gametes are formed, certain epigenetic markers remain and are passed on to the offspring. The questions, which are currently being researched, are how much and which part of the epigenetic information is preserved and subsequently inherited.
  • Diet and epigenetics appear to be closely linked. The most well known example is that of the Agouti mice: they are yellow, fat and are prone to diabetes and cancer. If Agouti females are fed with a cocktail of vitamin B12, folic acid and cholin, directly prior to and during pregnancy, they give birth to mainly brown, slim and healthy offspring. They in turn mainly have offspring similar to themselves.
  • Environmental factors, which change the characteristics of an individual and are then passed on to its offspring, do not really fit into Darwin’s theory of evolution. According to his theory, evolution is the result of the population and not the single individual. “Passing on the gained characteristics fits more to Lamarck’s theory of evolution”, says Paro.
nidthamsirisup

Study suggests why some animals live longer - 1 views

    • nidthamsirisup
       
      A new method to detect proteins associated with longevity which helps further our understanding into why some animals live longer than others.
  • The study, led by Dr. Joao Pedro Magalhaes and postgraduate student, Yang Li, is the first to show evolutionary patterns in biological repair systems in long-lived animals and could, in the future, be used to help develop anti-ageing interventions by identifying proteins in long-lived species that better respond to, for example, DNA damage
  • these species have optimised pathways that repair molecular damage, compared to shorter-lived animals, such as mice
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  • found a similar pattern in proteins associated with metabolism, cholesterol and pathways involved in the recycling of proteins
  • Proteins associated with the degradation of damaged proteins, a process that has been connected to ageing, were also linked with the evolution of longevity in mammals.
  • If we can identify the proteins that allow some species to live longer than others we could use this knowledge to improve human health and slow the ageing process.
  • “We developed a method to detect proteins whose molecular evolution correlates with longevity of a species. The proteins we detected changed in a particular pattern, suggesting that evolution of these proteins was not by accident, but rather by design to cope with the biological processes impacted by ageing, such as DNA damage. The results suggest that long-lived animals were able to optimise bodily repair which will help them fend off the ageing process.”
chanon chiarnpattanodom

Cancer epigenetics takes center stage - 1 views

    • chanon chiarnpattanodom
       
      DNA methylation is a chemical process where a methyl group is added on either the cytosine ring or the adenine ring, used in "higher leveled" organisms. Important in cell differentiation since methylation will cause cells to "remember" and remain differenciated instead of expressing other genes. 
  • Epigenetics is defined as modifications of the genome, heritable during cell division, that do not involve a change in the DNA sequence.
  • Epigenetic alterations in cancer include global hypomethylation
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  • the promoters of housekeeping genes that are generally protected from methylation.
  • may lead to aberrant silencing of tumor suppressor genes
  • discovered loss of imprinting (LOI) in cancer
  • Genomic imprinting, the subject of the report by Nakagawa et al. (2), is an epigenetic modification of a specific parental allele of a gene, or the chromosome on which it resides, in the gamete or zygote, leading to differential expression of the two alleles of the gene in somatic cells of the offspring.
  • we found that LOI can occur in the normal colonic mucosa of colorectal cancer patients with LOI in their tumors
  • This LOI was linked to cases showing microsatellite instability (MSI) in the tumors
  • However, these patients do not have mutations in mismatch repair genes
  • One potential cause of MSI in these sporadic cancers is hypermethylation and epigenetic silencing of the hMLH1 mismatch repair gene
  • Nakagawa et al. (2) now confirm the original study of Cui et al. that LOI occurs in both tumor and normal tissue of patients
  • The present study (2) also offers an intriguing mechanistic hypothesis to explain the relationship between H19 DMR methylation and LOI in these patients
  • Nevertheless, the study calls attention to this remarkable highly conserved multifunctional protein,
  • The potential link to CTCF suggested by this study also calls our attention to the link among DNA methylation, epigenetics, and chromatin.
  • A clue to the link between MSI and epigenetics may be provided by another sometimes overlooked common thread in epigenetics, namely DNA replication
  • repeat-induced gene silencing is thought to be propagated through hemimethylated intermediates during DNA replication
  • The studies of Cui et al. (11), Nishihara et al. (20), and Nakagawa et al. (2) suggest a new and provocative view of the timing of epigenetic changes in cancer.
  • Studies of transgenic mice with constitutive biallelic expression of IGF2, comparable to LOI, show reduced apoptosis and increased tumor formation
  • I conclude by noting that the distinction between cancer genetics and epigenetics has blurred considerably in recent years
  • Many conventional “genetic” mechanisms directly affect proteins that regulate chromatin,
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