Clinical Research in Cardiology

, Volume 96, Issue 5, pp 258–263

Hormonal status modulates circulating endothelial progenitor cells

Authors

  • Daniel Bulut*
    • Div. of CardiologySt. Josef-Hospital, Ruhr-University Bochum
  • Nadine Albrecht*
    • Div. of CardiologySt. Josef-Hospital, Ruhr-University Bochum
  • Matthias Imöhl
    • Institute for Clinical Chemistry and Laboratory MedicineBergmannsheil
  • Bülent Günesdogan
    • Div. of CardiologySt. Josef-Hospital, Ruhr-University Bochum
  • Nadine Bulut-Streich
    • Div. of CardiologySt. Josef-Hospital, Ruhr-University Bochum
  • Jan Börgel
    • Div. of CardiologySt. Josef-Hospital, Ruhr-University Bochum
  • Christoph Hanefeld
    • Div. of CardiologySt. Josef-Hospital, Ruhr-University Bochum
  • Michael Krieg
    • Institute for Clinical Chemistry and Laboratory MedicineBergmannsheil
    • Div. of CardiologySt. Josef-Hospital, Ruhr-University Bochum
ORIGINAL PAPER

DOI: 10.1007/s00392-007-0494-z

Cite this article as:
Bulut*, D., Albrecht*, N., Imöhl, M. et al. Clin Res Cardiol (2007) 96: 258. doi:10.1007/s00392-007-0494-z

Abstract

Objective

Endothelial progenitor cells (EPCs) may have an important role in vascular homeostasis and repair.

Methods

We examined the level of circulating EPCs in pre- (n = 22; mean age 28.7 years), and postmenopausal healthy females without (n = 30; mean age 61.6 years) or under current hormone replacement therapy (HRT) (n = 19; mean age 59.8 years).

Results

Premenopausal females had the highest level of circulating EPCs (0.147 ± 0.076‰ of polymorphnuclear cells). The level of EPCs was lowest in postmenopausal females (0.094 ± 0.058‰), and increased significantly with HRT on average by 25.5%. In addition, the proliferative capacity of circulating EPCs was assessed under cell culture conditions. This capacity was significantly increased in EPCs isolated from postmenopausal subjects under current HRT as compared to corresponding samples obtained from postmenopausal females without HRT.

Conclusions

This observation is in line with the hypothesis that the hormonal status in females modulates the cardiovascular risk and that circulating EPCs could be involved in this phenomenon.

Key words

endothelial progenitor cellscardiovascular riskendothelial functionhormone replacement therapyestradiol

Copyright information

© Steinkopff-Verlag 2007