Transcriptomics

Dataset Information

14

Accumulating mitochondrial DNA mutations drive premature hematopoietic aging phenotypes molecularly distinct from physiologic stem cell aging


ABSTRACT: Somatic stem cells mediate tissue maintenance for the lifetime of an organism. Despite the well-established longevity that is a prerequisite for such function, accumulating data argue for compromised stem cell function with age. Identifying the mechanisms underlying age-dependent stem cell dysfunction is therefore key to understand the aging process. Using a model that carries a proofreading defective mitochondrial DNA polymerase, we demonstrate hematopoietic defects reminiscent of premature HSC aging including anemia, lymphopenia and myeloid lineage skewing. However, in contrast to physiologic stem cell aging, rapidly accumulating mitochondrial DNA mutations displayed little involvement of the hematopoietic stem cell pool but rather with distinct differentiation blocks and/or disappearance of downstream progenitors. Hematopoietic stem cells (HSC) has been sorted out from midaged wildtype and mutator mice and compared with stem cells sorted from young and and old wt mice

ORGANISM(S): Mus musculus  

SUBMITTER: Amol Ugale   Cornelis J Pronk  Gudmundur L Norddahl  David Bryder  Gerd Sten  Jens M Nygren  Gudmundur Norddahl  Mikael Sigvardsson  Martin Wahlestedt 

PROVIDER: E-GEOD-27686 | ArrayExpress | 2011-05-06

SECONDARY ACCESSION(S): GSE27686PRJNA138165

REPOSITORIES: GEO, ArrayExpress

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Publications

Accumulating mitochondrial DNA mutations drive premature hematopoietic aging phenotypes distinct from physiological stem cell aging.

Norddahl Gudmundur L GL   Pronk Cornelis J CJ   Wahlestedt Martin M   Sten Gerd G   Nygren Jens M JM   Ugale Amol A   Sigvardsson Mikael M   Bryder David D  

Cell stem cell 20110501 5


Somatic stem cells mediate tissue maintenance for the lifetime of an organism. Despite the well-established longevity that is a prerequisite for such function, accumulating data argue for compromised stem cell function with age. Identifying the mechanisms underlying age-dependent stem cell dysfunction is therefore key to understanding the aging process. Here, using a model carrying a proofreading-defective mitochondrial DNA polymerase, we demonstrate hematopoietic defects reminiscent of prematur  ...[more]

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