Maternal Insulin Therapy Increases Fetal Endothelial Progenitor Cells during Diabetic Pregnancy
- Gian Paolo Fadini, MD (gianpaolofadini{at}hotmail.com)1,
- Ilenia Baesso, BSc1,
- Carlo Agostini, MD1,
- Emily Cuccato, Obst2,
- Giovanni Battista Nardelli, MD2,
- Annunziata Lapolla, MD3 and
- Angelo Avogaro, MD, PhD1
- 1Department of Clinical and Experimental Medicine
- 2Department of Gynecological Science and Human Reproduction
- 3Department of Medical and Surgical Sciences; All at the University of Padova (Italy), Medical School
Abstract
Abstract Endothelial progenitor cells (EPCs) are bone marrow-derived cells involved in endothelial homeostasis and angiogenesis. Reduction and dysfunction of EPCs have been associated with the development of atherosclerosis and diabetic complications (1; 2).
Abstract Recent studies in human pregnancies suggest that mother's EPCs are involved in the physiologic vascular remodelling of the systemic and utero-placental circulation (3; 4). Hyperglycemia induces dysfunction and apoptosis of EPCs (5), and this may impair the development or maturation of the utero-placental circulation, causing maladaptive responses during diabetic pregnancies. Indeed, EPCs has been shown to be dysregulated in pregnant women with diabetes (4).
Abstract On the other side, little is known on the effects of maternal factors on fetal EPCs. One study showed reduced cord blood EPCs in severe pre-eclampsia (6), while there are no data on diabetes. This study was undertaken to evaluate quantitative alterations of cord blood progenitor cells during pregnancies with diabetes mellitus.
Footnotes
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- Received October 15, 2007.
- Accepted December 17, 2007.
- Copyright © American Diabetes Association
