Melov Lab
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Simon Melov, Ph.D., Associate Professor and Director of the Genomics Core

Mitochondrial oxidative stress and aging

Simon Melov, Ph.D., focuses on understanding how production of damaging free radicals from within the mitochondria, the powerhouse of the cell, influences aging and age-related diseases. One of the chief tools used in the Melov laboratory is the “sod2 null” mouse. This mouse lacks the mitochondrial version of an essential protein for detoxifying a damaging free radical produced as a result of normal metabolic processes. A deficiency in this protein can cause a complex series of pathologies which affect multiple tissues including the heart, brain, and many other organs.

Other areas of study within the Melov lab involve characterizing pathological changes with age in the simple nematode Caenorhabditis elegans or “the worm.” C.elegans is arguably the preeminent invertebrate model of aging, and although its lifespan can be routinely extended through genetics or drugs, very little is known about its physiology as it ages. Therefore, the Melov lab is characterizing in detail the pathology of aging worms.

The lab is also devoting considerable effort to characterize genetic “fingerprints” of aging in multiple species including human beings. As organisms age, there are substantial changes in the expression of genes within each tissue. The expression profile, or “transcriptome” can be diagnostic of physiological or chronological age. In conjunction with collaborators, the Melov lab has identified specific gene expression profiles, or fingerprints which are capable of differentiating young animals from old animals, and even for predicting the age of the animal. This approach relies on the technology of gene expression profiling via microarrays, or “gene chips.” The Melov lab is also applying this technology to investigate how exercise benefits different tissues across the lifespan. This is exemplified in a recent study which showed that exercise in older individuals reversed specific aspects of the genetic “fingerprint” back to that of younger individuals.

 

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