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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:2099.)
© 2008 American Heart Association, Inc.

Editorials

Affirmative Action of Osteopontin on Endothelial Progenitors

Daniel G.M. Molin; Nynke M.S van den Akker; Mark J. Post

From the Departments of Physiology (D.G.M.M., M.J.P.) and Cardiology (N.M.S.v.d.A.), CARIM, Maastricht University Medical Center, the Netherlands; and the Department of Biomedical Engineering (M.J.P.), Eindhoven University of Technology, Eindhoven, the Netherlands.

Correspondence to Mark J. Post, MD, PhD, Department of Physiology, University Maastricht, PO Box 626, 6200 MD Maastricht, the Netherlands. E-mail m.post@fys.unimaas.nl

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Gender differences in susceptibility to coronary heart disease have been firmly established: the incidence of various manifestations of coronary atherosclerosis is less in premenopausal women than age-matched men. The protective role of estrogen covers a broad range of mechanisms including improvement of endothelial regeneration after arterial injury. Mediated primarily by the estrogen receptor alpha (ER), 17β-estradiol (E2) stimulates migration and proliferation of endothelium. This effect involves among others, eNOS activity,¹ prostacyclin, endothelin, bFGF,² and VEGF-R2 signaling.³ Estrogen also stimulates the recruitment of endothelial progenitor cells (EPCs), which in experimental and emerging clinical studies appear to be important effectors of endothelium repair (for review see Besler et al⁴). In rodents, E2 increases the number of circulating EPCs and enhances their adherence and homing to the region of vascular damage. This process is ER dependent and EPCs are believed to play a nonredundant role in the E2 enhanced reendothialization.¹ Likewise, in premenopausal women a higher number of circulating EPCs is found when compared to age-matched men. The level of circulating EPCs synchronizes with menstrual cycle and is the highest during the fertile period. In addition, male EPCs showed a lower adherence capacity as compared to premenopausal female EPCs, an effect that was abolished by E2 supplementation.⁵

See accompanying article on page 2131

The presumed clinical relevance of EPC recruitment, for instance in restenosis, is underscored by several strategies to arm stents with integrins or antibody based agents to enhance EPC homing and adherence. The mechanism of EPC enhanced reendothelialization, however, . . . [Full Text of this Article]

Related Article:

Estrogen-Stimulated Endothelial Repair Requires Osteopontin

Laetitia Lam Shang Leen, Cédric Filipe, Audrey Billon, Barbara Garmy-Susini, Sandra Jalvy, Fanny Robbesyn, Danièle Daret, Cécile Allières, Susan R. Rittling, Nikos Werner, Georg Nickenig, Urban Deutsch, Cécile Duplàa, Pascale Dufourcq, Françoise Lenfant, Claude Desgranges, Jean-François Arnal, and Alain-Pierre Gadeau
Arterioscler Thromb Vasc Biol 2008 28: 2131-2136. [Abstract] [Full Text] [PDF]