Decreased Endothelial Progenitor Cells in Preeclampsia and Consequences for Developmental Programming
See related article, pp 165–171
It has been ≈2 decades since the seminal report by Asahara et al,1 characterizing the isolation of endothelial progenitor cells (EPCs) from peripheral blood. Despite considerable debate on the most appropriate antigens for true identification of EPCs, several lines of evidence have emerged to show that they are recruited to sites of vascular lesions and may play a critical role in the repair of blood vessel damage, restoration of endothelial function, or neoangiogenesis after the fetal period.1,2 Although endothelial cell dysfunction is a hallmark of many cardiovascular diseases (including preeclampsia) and a growing body of literature suggests that reductions in the number and functionality of circulating EPCs play a role in adult cardiovascular diseases,2,3 whether alterations in EPCs contribute to fetal programming of disease is unclear.
Evidence suggests that circulating EPCs are reduced in preeclampsia and may contribute to endothelial dysfunction in these patients, but it remains unclear whether this represents a causal relationship in the pathophysiology of preeclampsia or is a biomarker for individuals susceptible to developing the condition. Moreover, the exact role of EPCs in developmental abnormalities and fetal programming remains unknown. Thus, the study by Muñoz-Hernandez et al4 in the current issue of Hypertension seems to be the first to show that endothelial colony–forming cells (ECFCs), a subset of EPCs, are reduced in cord blood of preeclamptic pregnancies. This represents an intriguing finding and may be an important step toward identifying a putative mechanism for developmental programming in pregnancies affected by preeclampsia.
Preeclampsia is a common hypertensive disorder of pregnancy characterized by widespread endothelial dysfunction and vasoconstriction resulting from abnormalities in …