STEM CELLS AND AGING · Stem cell niche and asymmetric division in aging
FP7 — People (Marie Curie Actions)
- Duration
- 2013-09-01 → 2017-08-31
- EU contribution
- €100,000
- Participants
- 1
- Scheme
- MC-CIG
Lines connect the coordinator with its partners.
Results in brief
Stem cell niche and asymmetric division in aging
Aging is caused by the time dependent accumulation of cellular damage. Such damage can impair tissue renewal in two ways: damage accumulation into the stem cells them selves can cause stem cell exhaustion, or damage to the stem cell niche can change the intercellular communication and the ability of stem cells to respond to cues guiding tissue homeostasis. The project “Stem cells and aging” set to support the initiation of an independent career of the fellow in University of Helsinki, and to investigate 1) how niche-stem cell interactions are changed during aging and 2) if stem cells use asymmetric cell division to quality control their organelles and counter aging. During the granting period, the fellow first received a tenure track Group Leader, and then a Tenure track Associate Professor position in the host institute. He now runs his own laboratory with >10 full time scientists and is fully integrated into the host institute as a principal investigator. The fellow has also made considerable progress regarding the two scientific aims. He has discovered multiple aging-related defects in the niche-stem cell communication that may impact stem cell activity. The first manuscript on these findings is in revision, and several others are in preparation. Currently the fellow is pursuing these leads to address their relevance for the reduced renewal and regeneration of aging tissues. Regarding the aim 2), the fellow discovered that stem cells indeed segregate at least certain organelles age-selectively and asymmetrically in cell division. This finding was published in the journal Science in 2015. The fellow is now continuing mechanistic studies regarding this novel phenomenon.
Data: CORDIS, © European Union
Project objective
Adult stem cells maintain tissues for the life of an organism by balancing regeneration with tissue damage and turnover. Accordingly, the functional decline associated with aging is hypothesized to result from the reduced net stem cell function. Mechanisms that increase stem cell number, maintenance, or function could therefore be used to counter age related tissue damage. Surprisingly, the very properties that set stem cells apart from all other cells have not been studied extensively in the context of aging. I will study whether the stem cell niche, or asymmetric cell division have roles in aging.Stem cells are surrounded by the niche cells that provide stem cells with factors regulating proliferation and differentiation. I have discovered that the intestinal stem cell niche couples stem cell function to the organismal nurient status during Calorie Restriction (CR) and increases stem cell number via a paracrine mechanism. As CR extends the lifespan and inhibits aging related phenotypes in multiple organisms, I will investigate whether niche mediated mechanisms can oppose the functional decline of the aging intestine.Stem cells generate two daughter cells with distinct fates in asymmetric cell division. It is conceivable that stem cells may asymmetrically apportion old and damaged cellular material to the differentiating progeny to secure the stem cell lineage. I have developed a method to address the age dependent apportioning of organelles in cell division, and discovered that the mammary progenitor cells dispose certain organelles age-dependently to the differentiating daughter. I will determine the role of this new mechanism in stem cell biology and aging.
Original text from CORDIS.
Participants
- HELSINGIN YLIOPISTO · HelsinkiCoordinatorFinland
Links
Data: CORDIS, © European Union