About Careers Internship MedBlogs Contact us
Medindia LOGIN REGISTER
Advertisement

Gene May Regulate Cellular Aging

by Rajshri on September 10, 2006 at 2:18 PM
Font : A-A+

Gene May Regulate Cellular Aging

A gene that has the potential to suppress tumor growth also plays a major role in aging, according to three separate studies. The gene p16INK4a caused cell to grow old and work poorly as compared to younger cells. These older cells seemed to know their age even when transplanted into young mice. Other cells in the young mice were not as sluggish as these older cells.

Teams from the medical schools at the University of North Carolina at Chapel Hill, University of Michigan and Harvard University observed similar results in pancreatic islet cells and brain and blood stem cells.

Advertisement

The results show disparate cell types share a common aging mechanism and suggest that aging-related diseases such as diabetes result from a failure of cell growth, said Dr. Norman E. Sharpless, co-author on the three studies and an assistant professor of medicine and genetics at the UNC School of Medicine. 'The studies indicate that certain stem cells lose their ability to divide and replace themselves with age as the expression of p16INK4a increases,' said Sharpless, a member of the UNC Lineberger Comprehensive Cancer Center.

The trio of reports are published online Sept. 6 in the journal Nature. The three research teams are from the medical schools at UNC, the University of Michigan and Harvard University.
Advertisement

The UNC study focused on p16INK4a effects on the function of pancreatic islet cells. Islet cells are responsible for insulin production and secretion. Because p16INK4a stops cancer cells from dividing and demonstrates increased expression with age, the scientists suspected the gene played a similar role in aging. The researchers developed strains of mice that were either deficient in p16INK4a (the gene was deleted, or 'knocked out') or genetically altered to have an excess of the protein to a degree seen in aging. According to Sharpless, islet proliferation persisted in p16INK4a -deficient animals as they aged, 'almost as if they were younger animals.' In mice with an excess of p16INK4a, 'islet cells aged prematurely; they stopped dividing early.' 'This suggests that if we could attenuate p16INK4a expression in some way in humans, it could lead to enhanced islet re-growth in adults and a possible new treatment for diabetes,' Sharpless said.

Similar results were found in the other studies, which focused on brain stem cells and blood stem cells.

The Michigan researchers, led by Dr. Sean Morrison, examined the role played by p16INK4a in neural stem cells, progenitor cells that can form new neurons and other brain cells. The team showed that p16INK4a increases markedly in those cells with aging. Moreover, p16INK4a -deficient neural stem cells work better and don't age to the same extent that wild-type (normal) stem cells do, Sharpless said.

Dr. Janakiraman Krishnamurthy, lead author of the UNC study and a postdoctoral scientist in the Sharpless lab, was a co-author of the Michigan report. The Harvard team, led by Dr. David Scadden, studied the role of p16INK4a in hematopoietic stem cells, which proliferate continuously during the adult lifespan and produce massive amounts of new blood cells on an hourly basis. Their results suggest that p16INK4a is the molecular basis for an old-age 'signal' previously observed in blood stem cells. The Harvard study also showed that blood stem cells from old mice lacking p16INK4a functioned better than old cells from wild-type mice, suggesting p16INK4a causes aging of these cells as well.

Sharpless cautions that any promise of a potential new aging treatment based on p16INK4a should include two important caveats. 'First, even though old mice lacking p16INK4a show enhanced stem cell function, they do not live longer. This is because p16INK4a is an important cancer-suppressor gene, and mice lacking p16INK4a develop more cancers than old, normal mice,' he said.

'Secondly, in all three studies, p16INK4a loss was associated with an improvement in some but not all of the consequences of aging. There are clearly things in addition to p16INK4a that contribute to aging. We don't yet know what they are.'

However, the gene may prove immediately useful as a biomarker for studies of aging, Sharpless said. 'If you were going to calorically restrict yourself or take green tea or resveratrol every day for years in an effort to prevent aging, wouldn't you like some evidence that these not entirely benign things were having a beneficial effect? Now we have a biomarker that can directly test the effects of such things,' he said.

Source: Eurekalert
RAS
Advertisement

Advertisement
News A-Z
A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
What's New on Medindia
Monkeypox Outbreak: What it is, How Does it Spread & the Prevention
Seasonal Allergy Medications
How to Choose the Best Eczema-Friendly Moisturizer for Children?
View all
Recommended Reading
News Archive
Date
Category
Advertisement
News Category

Medindia Newsletters Subscribe to our Free Newsletters!
Terms & Conditions and Privacy Policy.

More News on:
Ageing and Sleep 

Most Popular on Medindia

Blood - Sugar Chart Drug - Food Interactions Loram (2 mg) (Lorazepam) Diaphragmatic Hernia A-Z Drug Brands in India Accident and Trauma Care Iron Intake Calculator Find a Doctor Color Blindness Calculator Drug Side Effects Calculator

Disclaimer - All information and content on this site are for information and educational purposes only. The information should not be used for either diagnosis or treatment or both for any health related problem or disease. Always seek the advice of a qualified physician for medical diagnosis and treatment. Full Disclaimer

© All Rights Reserved 1997 - 2022

This site uses cookies to deliver our services. By using our site, you acknowledge that you have read and understand our Cookie Policy, Privacy Policy, and our Terms of Use