Difference between revisions of "Aging stem cells niches"

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Latest revision as of 09:26, 2 August 2015

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

Aging stem cells niches

Stem cell niches are composed of microenvironmental cells that nurture stem cells and enable them to maintain tissue homeostasis. An appropriate spatiotemporal dialog occurs between stem and niche cells in order to fulfill lifelong demands for differentiated cells. Niche cells provide a sheltering environment that sequesters stem cells from differentiation stimuli, apoptotic stimuli, and other stimuli that would challenge stem cell reserves. The niche also safeguards against excessive stem cell production that could lead to cancer. Stem cells must periodically activate to produce progenitor or transit amplifying (TA) cells that are committed to produce mature cell lineages. Thus, maintaining a balance of stem cell quiescence and activity is a hallmark of a functional niche.

Support cells within the niche influence stem cell function via direct interaction of membrane proteins present on the apposing cells, and also by the secretion of soluble factors and extracellular matrix components that bind to integral proteins expressed by stem cells and modulate their behavior.

The impairment in tissue homeostasis, repair, and regeneration with age is largely attributed to a decline in the ability of resident stem cells in individual tissues to efficiently and effectively give rise to new parenchymal cells. Changes in intrinsic factors, the niche microenvironment, or the systemic environment can lead to an aged phenotype of stem cells. Conversely, changes in stem cell function may also have an impact on the physiological status of an individual, possibly creating positive or negative feedback loops during aging. Aging of the niche has also been proposed to contribute to the decline in stem cell function with age. The physiological changes that result from aging can also impact stem cells and their niches. In old mice, muscle regeneration is impaired due to insufficient levels of Notch signaling in satellite cells, and forced activation of Notch is sufficient to restore efficient regeneration of older muscle. Intriguingly, exposure of old muscle to the systemic environment of a young mouse in heterochronic parabiosis is sufficient to restore Notch signaling and efficient satellite cell activation in older muscle.