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Caloric restriction does not alter effects of aging in cardiac side population cells

Jacob D Mulligan1, Eric G Schmuck, Rebecca L Ertel

  • 1Department of Medicine, University of Wisconsin-Madison, Madison, WI 53706, USA.

Age (Dordrecht, Netherlands)
|October 6, 2010
PubMed

Insights

Aging increases cardiac side population (CSP) cells but impairs their differentiation. Caloric restriction did not alter these aging effects in CSP cells, suggesting distinct aging mechanisms.

Area of Science:

  • Cardiovascular Biology
  • Aging Research
  • Stem Cell Biology

Background:

  • The aged heart exhibits cardiomyocyte loss and functional decline.
  • Cardiac progenitor cells may undergo senescence and reduced regeneration with age.
  • Cardiac side population (CSP) cells, a potential cardiac progenitor, remain unstudied in aging.

Purpose of the Study:

  • To investigate the impact of aging on CSP cells.
  • To determine if caloric restriction (CR) diet affects CSP cell aging.
  • To characterize age-related changes in CSP cell proliferation, senescence, and differentiation.

Main Methods:

  • Isolation of CSP cells from adult and aged mice using flow cytometry-assisted cell sorting.
  • Analysis of CSP cell subpopulations, including the cardiomyogenic sca1(+)/CD31(-) group.
  • Assessment of proliferation markers, senescence, telomerase activity, cell cycle genes, and differentiation gene expression.

Main Results:

  • Aging increased total CSP cells (2.3-fold) and the cardiomyogenic subpopulation (3.2-fold).
  • Aged sca1(+)/CD31(-) CSP cells showed no changes in proliferation or senescence markers.
  • Aged CSP cells exhibited reduced expression of differentiation genes (smooth muscle actin and cardiac muscle actin).
  • Caloric restriction did not modify any observed age-related effects on CSP cells.

Conclusions:

  • Aging alters CSP cell number and differentiation potential, distinct from other progenitor cells.
  • The aging of CSP cells is not attenuated by caloric restriction.
  • These findings suggest unique aging mechanisms in cardiac progenitor cells impacting cardiac health.

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