Abstract
Although neurogenesis occurs in discrete areas of the adult mammalian brain, neural progenitor cells (NPCs) produce fewer new neurons with age. To characterize the molecular changes that occur during aging, we performed a proteomic comparison between primary-cultured NPCs from the young adult and aged mouse forebrain. This analysis yielded changes in proteins necessary for cellular metabolism. Mitochondrial quantity and oxygen consumption rates decrease with aging, although mitochondrial DNA in aged NPCs does not have increased mutation rates. In addition, aged cells are resistant to the mitochondrial inhibitor rotenone and proliferate in response to lowered oxygen conditions. These results demonstrate that aging NPCs display an altered metabolic phenotype, characterized by a coordinated shift in protein expression, subcellular structure, and metabolic physiology.
Highlights
Mitochondrial dysfunction occurs in many tissues during normal aging
We present the first comparative proteomic analysis between young and aged neural progenitor cells (NPCs), which yielded age-related changes in abundance of proteins involved in cellular metabolism
These data agree with previous results demonstrating that fewer numbers of NPCs in aged cultures are capable of forming neurosphere colonies [5]
Summary
Mitochondrial dysfunction occurs in many tissues during normal aging. Results: Aged neural progenitor cells (NPCs) have decreased regenerative capacity, fewer functional mitochondria, and less oxygen consumption compared with young adult NPCs. We present the first comparative proteomic analysis between young and aged NPCs, which yielded age-related changes in abundance of proteins involved in cellular metabolism In support of these results, we report the novel finding that aging NPCs have decreased mitochondrial mass, corresponding with lower oxygen consumption and increased resistance to mitochondrial inhibition. These findings have implications for the understanding of normal aging and agerelated pathologies, providing a potential mechanism by which aging NPCs could adapt to nutrient deprivation and hypoxia, with relevance to environmental conditions encountered in tumor and stroke.
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