Premature deliveries account for 10% of live births in the US and the survival of premature infants has improved over the years with advances in perinatal and neonatal care. Nearly 25-30% of premature infants with birth weight below 1250 grams develop bronchopulmonary dysplasia (BPD) characterized by abnormal alveolar and vascular development during a critical stage of postnatal lung development. Animal models of BPD suggest that abnormal lung microvascular development leads to the failure of alveolar development and strategies that promote vascular development result in improved alveolarization of the lung. In addition, low levels of bone marrow-derived and circulating endothelial progenitors have been observed in the blood of hyperoxia exposed neonatal mice that develop BPD, suggesting that bone marrow-derived endothelial progenitors may play a role in neonatal lung development. A human study reported lower levels of endothelial colony forming cells (ECFC) in cord blood from preterm infants who developed BPD than in cord blood from preterm infants who did not develop BPD . However, others have observed higher or equivalent numbers of ECFC counts in cord blood from preterm deliveries as compared to term cord blood. Our group recently reported that circulating endothelial progenitor cell frequency in human neonates in the first three weeks of life may be influenced by postnatal clinical stress.
Hisham Abdel-Azim, Circulating Endothelial Progenitors and Bone Marrow Derived Cells as Biomarkers for Risk of Bronchopulmonary Dysplasia
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Last date updated on July, 2014