• Perelman School of Medicine
• University of Pennsylvania Health System

• Cell Biology

• Cheating a Cell's Demise

• • News Bite

The lifespan of normal human cells is determined in part by telomeres – the DNA-protein structures that cap the beginnings and ends of chromosomes. Telomeres dwindle every time a cell divides, and when telomeres become critically short, cells will either die or stop dividing permanently, called cellular senescence. These events are important for understanding how to crack the code of the aging process – as well as how to fight cancer.

Telomeres (red tips). Credit: Brad Johnson, MD, PhD.

"Telomeres become short as people age and there is evidence that this drives aspects of aging. So it’s reasonable to think that if we can protect telomeres we'll be better able to treat such age-related diseases as atherosclerosis, osteoporosis, and immune dysfunction," says Brad Johnson, MD, PhD, assistant professor of Pathology and Laboratory Medicine at the University of Pennsylvania.

Johnson, together with Marina Kozak, Alex Chavez and colleagues reported in The EMBO Journal the first demonstration that cellular senescence caused by telomere shortening can be slowed by manipulating telomere chromatin. This is the DNA-protein complex that composes chromosomes.

Before this study, it was known that cellular senescence causes changes in telomere chromatin, but Johnson’s group demonstrated the converse: that manipulation of telomere chromatin can slow cell senescence. "This is significant because it’s easy to find ways to speed senescence, but it wasn't clear how easy it would be to slow down the process," says Johnson.

The study was performed in yeast, but it is known that the same sort of telomere chromatin changes that occur in yeast also happen in mice, and perhaps in humans. The protein that Johnson manipulated to slow senescence, Sas2, has a human counterpart called hMOF, prompting the group to start similar experiments in human cells.

This story appears in Penn Medicine's Basic Science News Bites (December 2009). Also in this edition:

• Orthopaedics Research
• Throwing Their Backs into Regenerative Medicine
• In order for tissue grown in the lab to replace damaged or diseased tissue in the body, it needs to withstand complex mechanical loads – large forces regularly experienced over a lifetime of daily activities.
• • News Bite

• Cell Biology
• Cheating a Cell's Demise
• The lifespan of normal human cells is determined in part by telomeres – the DNA-protein structures that cap the beginnings and ends of chromosomes.
• • News Bite

• Neuroscience Research
• Prion-Busting Cocktails
• Prions are proteins that act like germs, infecting healthy tissue and causing havoc in the body. Their extreme stability and shape-shifting abilities make prions exceptionally difficult drug targets.
• • News Bite

• Aging Research
• New System to Find Parkinson's Disease Drugs
• There are a million ways to muck up a nerve cell. In the case of Parkinson’s disease, Lewy bodies are abnormal clumps that develop inside brain cells.
• • News Bite

• Diabetes Research
• New Insights on Insulin Resistance
• The overwhelming majority of type 2 diabetics are insulin resistant, which means their bodies are unable to respond to and use the insulin they produce.
• • News Bite

• Cardiology Research
• Master-Switch Protein Required for Heart-Cell Survival
• Researchers have discovered a new molecular pathway controlled by a master-switch protein in the heart muscles called myocardin that may be key to understanding some forms of heart disease.
• • News Bite

• Genetics Research
• Zebrafish Model of Common Genetic Disorder
• Because zebrafish develop rapidly, are transparent when young, and can be easily bred in large numbers, this new animal model will dramatically increase the screening capacity for a common human inherited disorder.
• • News Bite

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