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HK scientists shed new light on aging process

Posted on: Thursday, 30 June 2005, 07:20 CDT

By Tan Ee Lyn

HONG KONG (Reuters) - Scientists in Hong Kong have shed newlight on why cell repair is less efficient in older peopleafter a breakthrough discovery on premature aging, a raregenetic disease that affects one in four million babies.

Premature aging, or Hutchison-Gilford Progeria Syndrome(progeria), is obvious in the appearance of a child before itis a year old. Although their mental faculties are normal, theystop growing, lose body fat and suffer from wrinkled skin andhair loss.

Like old people, they suffer stiff joints and a buildup ofplaque in arteries which can lead to heart disease and stroke.Most die of cardiovascular diseases before they are 20.

In 2003, a team of scientists in the United States foundthat progeria was caused by mutation in a protein called LaminA, which lines the nucleus in human cells.

A team at the University of Hong Kong, led by ZhouZhongjun, took the research a step further in 2004 and foundthat mutated Lamin A actually disrupted the repair process incells, thus resulting in accelerated aging.

The study was published in the July issue of the NatureMedicine journal.

Zhou said the team came by their findings after comparingskin cells taken from two progeria sufferers, normal humans,progeria mice and normal mice.

While damaged DNA was quickly repaired in the healthy humanand mice cell samples, the samples taken from the progeriahumans and mice had difficulty repairing damaged DNA.

"Mutation in this protein (Lamin A) can cause defects inrepair and thus lead to progeria," Zhou, a research assistantprofessor with the biochemistry department at the University ofHong Kong, said in an interview.

"DNA damage is not effectively repaired in cells withdefective Lamin A but very efficiently repaired in normalcells."

The study highlights the importance of Lamin A to therepair process, and any mutation to Lamin A that disruptsrepair will bring about aging, Zhou said.

Having established the link between Lamin A and repair,Zhou is using major findings from other research he did in 2002to work on his next project, a product which he hopes couldkill cancer cells.

Zhou, Professor Karl Tryggvason in Sweden's KarolinskaInstitute and a Spanish research group found in 2002 that theenzyme Zmpste 24 was responsible in converting prelamin A tofunctional Lamin A.

Zhou's laboratory is now developing inhibitors to Zmpste24, which he hopes to apply to tumors. These inhibitors shouldtheoretically disrupt Lamin A production, thwart the repairfunction in cancer cells, and bring on their premature agingand death.

"We're now trying to develop inhibitors to Zmpste 24 andapply it to tumor cells," he said.

Source: REUTERS

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