Estrogen-dependent endothelial progenitor cells (EPC) mobilization in fertile women: potentially vasoprotective effects.

S. GARIBALDI; M.S. GIRETTI; A. CARUSO; P. MANNELLA; C. BALDACCI; X.D. FU; M. FLAMINI; A.M. SANCHEZ; L. GOGLIA; S. PISANESCHI; A.R. GENAZZANI; T. SIMONCINI

8-11 March, Rome, Italy

Congreso; The 2nd World Congress on Gender-Specific Medicine and Ageing. The Endocrine Impact.; 2007

After the menopause, cardiovascular diseases (CVD) represent the first cause of mortality and morbidity in Western women. Therefore, estrogen deficiency has been associated to the esponential increase of atherosclerosis and coronary heart disease after menopause. Estrogen is essential for vascular integrity and function through direct and indirect action on vessels. Recently, estrogen has been demonstrated to regulate endothelial progenitor cells (EPC) mobilization from the bone marrow to the bloodstream. EPCs can home to sites of ischemia and contribute to neovascularization and regeneration of damaged tissue myocardial regeneration. Therefore in terms of cardiovascular diseases, an increase of EPCs could be considered potential benefit for vascular protection. In order to establish possible correlation between estrogen concentration and EPCs level, we counted the number of circulating EPC in randomly selected fertile or pregnant women. The number of EPCs positive for CD34, CD133 and VEGF receptor-2 was determined with the use of flow cytometry. Our data show that the number of EPCs in women is very low but small variations of estrogen correspond to statistically increase of circulating EPCs, especially in periovulatory period. It is important to note that in pregnant women the number of circulating EPC is very high and increases with the gestational age of the woman. Although EPCs role is largely unknown in no-reproductive tissues, our findings demonstrate estrogen concentrations deeply influence EPCs mobilization. By regulation of EPCs number, estrogen may regulate several protective effects on the cardiovascular system as well as repairing sites of damage at endothelial level.