liu.seSearch for publications in DiVA
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Accumulating Mitochondrial DNA Mutations Drive Premature Hematopoietic Aging Phenotypes Distinct from Physiological Stem Cell Aging
Immunology Section, Institution for Experimental Medical Science, Lund University.
Immunology Section, Institution for Experimental Medical Science, Lund University.
Immunology Section, Institution for Experimental Medical Science, Lund University.
Immunology Section, Institution for Experimental Medical Science, Lund University.
Show others and affiliations
2011 (English)In: CELL STEM CELL, ISSN 1934-5909, Vol. 8, no 5, 499-510 p.Article in journal (Refereed) Published
Abstract [en]

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 premature HSC aging, including anemia, lymphopenia, and myeloid lineage skewing. However, in contrast to physiological stem cell aging, rapidly accumulating mitochondria! DNA mutations had little functional effect on the hematopoietic stem cell pool, and instead caused distinct differentiation blocks and/or disappearance of downstream progenitors. These results show that intact mitochondrial function is required for appropriate multilineage stem cell differentiation, but argue against mitochondria! DNA mutations per se being a primary driver of somatic stern cell aging.

Place, publisher, year, edition, pages
Elsevier Science B.v; Amsterdam , 2011. Vol. 8, no 5, 499-510 p.
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-68918DOI: 10.1016/j.stem.2011.03.009ISI: 000290927600011OAI: oai:DiVA.org:liu-68918DiVA: diva2:422032
Available from: 2011-06-10 Created: 2011-06-10 Last updated: 2014-10-22

Open Access in DiVA

No full text

Other links

Publisher's full text

Authority records BETA

Sigvardsson, Mikael

Search in DiVA

By author/editor
Sigvardsson, Mikael
By organisation
Experimental HematologyFaculty of Health Sciences
Medical and Health Sciences

Search outside of DiVA

GoogleGoogle Scholar

doi
urn-nbn

Altmetric score

doi
urn-nbn
Total: 48 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf