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Tiny molecule controls stress-induced heart disease

03-22-2007 · EurekAlert!

A tiny snippet of RNA, a chemical cousin of DNA, controls damage to the heart under several types of stress, researchers at UT Southwestern Medical Center have found.

Keywords: tiny, molecule, controls, stress-induced, heart, disease, control, stress, induced

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Tiny molecule controls stress-induced heart disease
03-23-2007 · UT Southwestern Medical Center
A tiny snippet of RNA, a chemical cousin of DNA, controls damage to the heart under several types of stress, researchers at UT Southwestern Medical Center have found.
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Advance in understanding of blood pressure gene could lead to new treatments
02-04-2007 · EurekAlert!
Research by scientists at UCL (University College London) has clearly demonstrated for the first time the structure and function of a gene crucial to the regulation of blood pressure. The discovery could be important in the search for new treatments for illnesses such as heart disease, the UK's biggest killer. In a paper published online today in Nature Medicine, the team, led by Professor Patrick Vallance and Dr James Leiper, UCL Department of Medicine, reveal the role of the human gene dimethylarginine dimethylaminohydrolase (DDAH), showing that loss of DDAH activity disrupts nitric oxide (NO) production. NO is critical in the regulation of blood pressure, nervous system functions and the immune system. The role of DDAH is to break down modified amino acids (Asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA)) that are produced by the body and have been shown to inhibit NO synthase. These molecules accumulate in various disease states including diabetes, renal failure and pulmonary and systemic hypertension, and their concentration in plasma (the fluid component of blood) is strongly predicative of cardiovascular disease and death. In a healthy human body, the majority of ADMA is eliminated through active metabolism by DDAH. Scientists have hypothesised that if DDAH function is impaired, NO production is reduced, and that this could be an important feature of increased cardiovascular risk. To examine this pathway in more detail, the researchers deleted the DDAH gene in mice. These mice went on to develop hypertension, or high blood pressure. They also designed specific inhibitors (small molecules) which bind to the active site of human DDAH. These small molecule inhibitors also induced hypertension in mice, confirming the importance of DDAH in the regulation of blood pressure. Dr Leiper, UCL Medicine, said: “These genetic and chemical approaches to disrupt DDAH showed remarkably consistent results, and provide compelling evidence that loss of DDAH function increases the concentration of ADMA and thereby disrupts vascular NO signalling. “There has been considerable scientific interest in this pathway and the role of ADMA as a novel risk factor, but so far there's been little evidence to support the idea that it's a cause of disease, rather than just a marker. Genes and their pathways are crucial to our understanding of cardiovascular disease and a better understanding of DDAH-1 could lead to important new treatments. “It could help us to establish if genetic variation predisposes certain people to these diseases, or whether environmental factors exert some of their effects through modulation of DDAH activity. “Our research also shows that this pathway could be harnessed therapeutically to limit production of NO in certain situations where too much nitric oxide is a bad thing; for example, hypotension and septic shock. These are some of the biggest problems in intensive care medicine and there is a huge unmet need for drug treatments.” The study, which was carried out at UCL's Rayne Institute, was funded by grants from the British Heart Foundation, the Wellcome Trust and the Medical Research Council. Professor Jeremy Pearson, Associate Medical Director of the British Heart Foundation, said: "The unexpected finding in the 1980s that a simple gas, nitric oxide (NO), is made by cells in the blood vessel wall and is a powerful control of blood vessel relaxation led to the award of the Nobel Prize in 1998 to its discoverers. "More recently, there has been increasing evidence that impairment of NO production is likely to be an important factor in the development of heart and circulatory disease, but the mechanisms responsible are not fully understood. "This study suggests for the first time that the loss of the activity of the enzyme DDAH-1 leads to reduced NO production and may cause heart and circulatory disease. These findings are likely to be important in the search for new ways to optimise the health of our blood vessels." ### Notes for Editors 1. For more information, please contact Ruth Metcalfe in the UCL Media Relations Office on tel: +44 (0)20 7679 9739, mobile: +44 (0)7990 675 947, out of hours: +44 (0)7917 271 364, e-mail: r.metcalfe@ucl.ac.uk2. 'Disruption of methylarginine metabolism impairs vascular homeostasis' is published in the February issue of the journal Nature Medicine. Advance online publication is embargoed to 18.00 GMT (13.00 US Eastern) Sunday 4 February 2007. Journalists can obtain copies of the paper by contacting the UCL Media Relations Office.3. The study was funded by the British Heart Foundation, the Wellcome Trust and the Medical Research Council. About UCL Founded in 1826, UCL was the first English university established after Oxford and Cambridge, the first to admit students regardless of race, class, religion or gender, and the first to provide systematic teaching of law, architecture and medicine. In the government's most recent Research Assessment Exercise, 59 UCL departments achieved top ratings of 5* and 5, indicating research quality of international excellence. UCL is the fourth-ranked UK university in the 2006 league table of the top 500 world universities produced by the Shanghai Jiao Tong University. UCL alumni include Mahatma Gandhi (Laws 1889, Indian political and spiritual leader); Jonathan Dimbleby (Philosophy 1969, writer and television presenter); Junichiro Koizumi (Economics 1969, Prime Minister of Japan); Lord Woolf (Laws 1954, Lord Chief Justice of England & Wales); Alexander Graham Bell (Phonetics 1860s, inventor of the telephone), and members of the band Coldplay.
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Largest ever study of genetics of common diseases published today
06-06-2007 · EurekAlert!
The Wellcome Trust Case Control Consortium, the largest ever study of the genetics behind common diseases such as diabetes, rheumatoid arthritis and coronary heart disease, today publishes its results in the journals Nature and Nature Genetics. The study examined DNA samples from 17,000 people across the UK, bringing together 50 leading research groups and 200 scientists in the field of human genetics. Over two years, they analysed almost 10 billion pieces of genetic information.
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Dietary copper may ease heart disease
03-05-2007 · EurekAlert!
Including more copper in your everyday diet could be good for your heart, according to scientists at the University of Louisville Medical Center and the USDA Human Nutrition Research Center. Their studies show that giving copper supplements to mice eased the stress on their over-worked hearts by preventing heart enlargement. The study will be published online on March 5 in the Journal of Experimental Medicine.
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The future of medicine -- Insert chip, cure disease?
07-25-2007 · EurekAlert!
Imagine a chip, strategically placed in the brain, that could prevent epileptic seizures or allow someone to control an artificial arm just by thinking about it. It may sound like science fiction, but University of Florida researchers are developing devices that can stimulate neurons to perform correctly, advances that might make it possible for a tiny computer to fix diseases or allow a paralyzed person to control a prosthesis with his thoughts.
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Monkey studies parallel WHI findings, point to importance
06-25-2007 · EurekAlert!
Studies in female monkeys helped raise important questions about hormone therapy that were addressed in a Women's Health Initiative study reported last week in the New England Journal of Medicine. The animal research, conducted at the Wake Forest University Primate Center, also suggests the role that stress can play in heart disease development and point to the need for early prevention of heart disease.
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New studies on cancer and schizophrenia, depression and heart disease, trauma and autism
12-10-2007 · EurekAlert!
The 2007 American College of Neuropsychopharmacology Annual Meeting will feature hundreds of new studies on brain and behavior from the world’s leading scientists. Presentations include innovative research on potential new treatments for depression, post-traumatic stress disorder, autism and addiction.
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Enzyme structure reveals new drug targets for cancer and other diseases
02-14-2008 · EurekAlert!
Researchers now have a clearer understanding of how a key protein controls gene activity and how mutations in the protein may cause disease. The work could provide new avenues to design drugs aimed at cancer, diabetes, HIV, and heart disease.
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JCI table of contents: February 15, 2006
02-15-2007 · EurekAlert!
This release contains summaries, links to PDFs and contact information for the following newsworthy papers to be published online, February 15, 2006, in the JCI, including: Protein inhibitor tangles with Alzheimer's disease; Proteases cause pain in irritable bowel syndrome; The "shear stress" of it impacts heart disease; Blood pressure heads down in the absence of PPAR-gamma; and Profiling peripheral T cell lymphoma for clues to its pathogenesis.
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Study of Whitehall civil servants explains how stress at work is linked to heart disease
01-22-2008 · EurekAlert!
New research published in the European Heart Journal has produced strong evidence of how work stress is linked to the biological mechanisms involved in the onset of heart disease. It is the first large-scale study to look at the cardiovascular mechanisms of work stress in the population and provides the strongest evidence yet of the way it can lead to coronary heart disease, either directly, by activating stress pathways controlled by neuroendocrine mechanisms, or indirectly via its association with unhealthy lifestyles.
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