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Regulation of circulating progenitor cells in left ventricular dysfunction

Barry A Boilson1, Katarina Larsen, Adriana Harbuzariu

  • 1Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, Rochester, Minn, USA.

Circulation. Heart Failure
|June 25, 2010
PubMed

Insights

Mineralocorticoid excess, from conditions like high blood pressure, reduces hematopoietic progenitor cells (HPCs). This suggests mineralocorticoids accelerate progenitor cell aging, decreasing their numbers in cardiovascular disease risk.

Area of Science:

  • Cardiovascular Biology
  • Hematology
  • Endocrinology

Background:

  • Circulating progenitor cells, including CD34+ cell subsets, are reduced in cardiovascular disease (CVD).
  • The specific factors mediating these reductions in progenitor cells are not well understood.
  • Neurohumoral factors are investigated as potential regulators of progenitor cell populations in vivo.

Purpose of the Study:

  • To investigate the role of neurohumoral factors, specifically mineralocorticoids, in regulating circulating progenitor cells.
  • To determine the effect of left ventricular (LV) dysfunction on progenitor cell subsets.
  • To assess the impact of mineralocorticoid excess on hematopoietic progenitor cells (HPCs) and endothelial progenitor cells (EPCs).

Main Methods:

  • Utilized canine models of left ventricular (LV) dysfunction, including pacing-induced and hypertensive renal wrap models.
  • Quantified circulating CD34+ cell subsets, specifically HPCs (CD34+/CD45(dim)/VEGFR2-) and EPCs (CD34+/CD45-/VEGFR2+).
  • Administered deoxycorticosterone acetate (DOCA) to normal dogs to study the effects of exogenous mineralocorticoid excess.

Main Results:

  • Pacing-induced LV dysfunction led to a decrease in HPCs, correlating with plasma aldosterone levels.
  • Mineralocorticoid excess induced by DOCA administration significantly reduced HPCs in peripheral blood.
  • No significant changes were observed in endothelial progenitor cells (EPCs) in either model.
  • DOCA treatment in normal dogs decreased HPCs in peripheral blood but not bone marrow, linked to reduced telomerase activity.

Conclusions:

  • This study demonstrates that both endogenous and exogenous mineralocorticoid excess reduce hematopoietic progenitor cells (HPCs).
  • Mineralocorticoids may accelerate the senescence of progenitor cells, leading to a decline in their numbers.
  • These findings suggest a novel mechanism linking mineralocorticoid activity to reduced progenitor cell populations in conditions like cardiovascular disease.
Abstract

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