Wednesday, May 2, 2012

Singapore - Scientists find new developments to treat heart diseases

SINGAPORE: Scientists at Singapore's Institute of Medical Biology (IMB) have made a discovery that could lead to the development of new treatments for heart diseases.

They discovered that they can dramatically increase the life span of mice with progeria premature ageing disease and heart disease caused by Emery-Dreifuss muscular dystrophy by reducing levels of a protein called SUN1.

The IMB, which is a biomedical sciences institute of the Agency for Science, Technology and Research (A*STAR), worked with the National Institute of Allergy and Infectious Diseases in the United States and the Institute of Cellular and System Medicine in Taiwan.

A*STAR said on Monday that their findings provide an exciting lead into developing new methods to treat premature aging and heart disease.

The findings were published in the prestigious scientific journal, Cell, on 27 April 2012.

Children with progeria suffer symptoms of premature ageing and mostly die in their early teens from either heart attack or stroke.

Individuals with Emery-Dreifuss muscular dystrophy (AD-EDMD) suffer from muscle wasting and cardiomyopathy, a type of heart disease that weakens and enlarges the heart muscle making it harder for the heart to pump blood and deliver it to the rest of the body leading to heart failure.

Both diseases are caused by mutations in Lamin A, a protein in the membrane surrounding a cell's nucleus which provides mechanical support to the nucleus.

SUN1 is a protein also found in the inner nuclear membrane, but there have been no previous studies to show how SUN1 interacts with the Lamin proteins.

The scientists wanted to investigate if SUN1 had any involvement in diseases caused by mutations in Lamin A, so they inactivated SUN1 in mouse models developed for progeria and AD-EDMD.

These mouse models for progeria and AD-EDMD usually thrive poorly and have markedly short life spans.

The mouse models for progeria die from premature ageing and while those for AD-EDMD die of heart failure.

The scientists inactivated SUN1 and reduced SUN1 levels in these mouse models and found that the life spans of the mouse models for progeria doubled while that of AD-EDMD tripled.

Principle Investigator at IMB, Professor Colin Stewart, said the heart muscle of the mice was restored to near-normal function.

He said cardiac function improved when the levels of SUN1 were reduced.

"This opens up a possibility that from these observations, reduction in SUN1 maybe of therapeutic use for other forms of heart disease. We are very excited about this discovery and look forward to further pursuing this lead which could potentially lead to development of new treatments for heart diseases," he said.

- CNA/ck

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