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Age-associated mitochondrial DNA mutations lead to small but significant changes in cell proliferation and apoptosis

Marco Nooteboom1, Riem Johnson, Robert W Taylor

  • 1Mitochondrial Research Group, Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.

Aging Cell
|November 3, 2009
PubMed

Insights

Mitochondrial DNA (mtDNA) mutations impair cell function in aging humans. Respiratory chain (RC) deficiency in colonic stem cells reduces proliferation and increases cell death, shrinking the crypt cell population.

Area of Science:

  • Cellular Biology
  • Genetics
  • Gerontology

Background:

  • Mitochondrial DNA (mtDNA) mutations are linked to human diseases and aging.
  • Clonally expanded mtDNA point mutations can cause respiratory chain (RC) defects in replicating tissues.

Purpose of the Study:

  • To investigate the impact of RC deficiency on human colonic epithelial stem cells and their progeny in elderly individuals.
  • To determine the consequences of RC defects on cellular functions beyond energy production.

Main Methods:

  • Analysis of human colonic epithelial stem cells from elderly individuals.
  • Assessment of cell proliferation and apoptosis in progeny of RC-deficient stem cells.

Main Results:

  • RC deficiency was observed in aging human colonic tissue.
  • RC deficiency significantly attenuates cell proliferation in the progeny of affected stem cells.
  • Increased apoptosis was detected in the progeny of RC-deficient stem cells.

Conclusions:

  • RC deficiency in colonic epithelial stem cells leads to reduced cell proliferation and increased apoptosis.
  • This cellular dysfunction results in a decreased crypt cell population in aging individuals.
  • mtDNA mutations causing RC defects have significant functional consequences in aging human tissues.

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