Abstract
Age-progressive neural stem cell (NSC) dysfunction leads to impaired neurogenesis, cognitive decline and the onset of age-related neurodegenerative pathologies. p38MAPK signalling pathway limits stem cell activity during aging in several tissues. Its role in NSCs remains controversial. In this work, we show that p38MAPK activity increases in NSCs with age in the subventricular zone (SVZ) and its pharmacological inhibition is sufficient to rejuvenate their activity in vitro. These data reveal a cell-autonomous role for p38MAPK increase in decreasing NSC homeostasis with age. This information shed light in the role of p38MAPK in NSC aging.
Highlights
Adult stem cells are responsible for the maintenance of tissue homeostasis during the life of the organism and this control is due to their specific characteristics of quiescence, self-renewal potential and capacity to differentiate to specialized cell lineages
We first determined the activity of p38 mitogen-activated protein kinase (p38MAPK) in young (2 month-old) and aged (≥ 2 year-old) subventricular zone (SVZ) from C57BL/6J mice
Immunofluorescence showed that p38MAPK phosphorylated in the activating residues (Pp38MAPK) was low in the cells along the SVZ in young mice and significantly increased in over 2 yearold animals (Figure 1A, 1B)
Summary
Adult stem cells are responsible for the maintenance of tissue homeostasis during the life of the organism and this control is due to their specific characteristics of quiescence, self-renewal potential and capacity to differentiate to specialized cell lineages. We first determined the activity of p38MAPK in young (2 month-old) and aged (≥ 2 year-old) SVZ from C57BL/6J mice.
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