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Published ahead of print on July 2, 2009, doi:10.1164/rccm.200812-1949OC
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American Journal of Respiratory and Critical Care Medicine Vol 180. pp. 540-546, (2009)
© 2009 American Thoracic Society
doi: 10.1164/rccm.200812-1949OC


Original Article

Circulating Endothelial Progenitor Cells in Preterm Infants with Bronchopulmonary Dysplasia

Alessandro Borghesi1, Margherita Massa2, Rita Campanelli3, Lina Bollani1, Chryssoula Tzialla1, Tiziana A. Figar1, Giovanna Ferrari1, Elisa Bonetti3, Gaia Chiesa1, Annalisa de Silvestri4, Arsenio Spinillo5, Vittorio Rosti6 and Mauro Stronati1

1 Neonatal Intensive Care Unit, 2 Biotechnology Laboratory, 3 Clinical Epidemiology Unit, 4 Department of Biometry and Statistics, 5 Department of Obstetrics and Gynecology, and 6 Organ Transplantation Laboratory, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy

Correspondence and requests for reprints should be addressed to Alessandro Borghesi, M.D., Fondazione IRCCS Policlinico San Matteo, Piazzale Golgi n. 19, 27100 Pavia, Italy. E-mail: alessandroborghesi{at}yahoo.it

Rationale: The new form of bronchopulmonary dysplasia (BPD) is characterized by lung immaturity with disrupted alveolar and capillary development after extremely premature birth, but the mechanism of impaired lung vascular formation is still not completely understood.

Objectives: We tested the hypothesis that reduced numbers of circulating endothelial progenitor cells at birth are associated with the development of BPD.

Methods: We studied ninety-eight preterm infants with gestational age of less than 32 weeks or a birth weight less than 1,500 g. Endothelial colony-forming cells (ECFCs) were assessed by clonogenic analysis in infants for whom cord blood was available. The proportion of circulating endothelial and hematopoietic cells was measured by flow cytometry at birth, at 48 hours, and at 7 days of life.

Measurements and Main Results: ECFCs in cord blood were lower in infants who later developed BPD (median [range]: 0.00 [0.00–0.48] vs. 2.00 [0.00–21.87]; P = 0.002). ECFCs decreased with decreasing gestational age (r = 0.41; P = 0.02), but even at extremely low gestational ages, infants with higher numbers of ECFCs were protected from BPD. The endothelial and hematopoietic cell subsets studied by flow cytometry were comparable in infants with and without BPD and rapidly decreased after birth.

Conclusions: ECFCs are low at extremely low gestational ages and increase during gestation; extremely preterm infants who display lower numbers at birth have an increased risk of developing BPD. Our findings suggest that decreased ECFCs following extremely preterm birth may be associated with the risk for developing lung vascular immaturity characteristic of new BPD.

Key Words: newborn • EPC • HPC • endothelial colony forming cell • chronic lung disease of prematurity


AT A GLANCE COMMENTARY

Scientific Knowledge on the Subject
Several risk factors predispose ventilated extremely preterm infants to the development of the new form of bronchopulmonary dysplasia (BPD), but the mechanism of impaired lung vascular formation is unknown.

What This Study Adds to the Field
In extremely preterm infants, lower numbers of circulating endothelial progenitor cells at birth are associated with an increased risk of developing BPD; this finding may be implicated in lung vascular immaturity observed in infants with BPD.

 

Related articles in AJRCCM:

Endothelial Progenitors in the Risk of Developing Bronchopulmonary Dysplasia: Can We Include Endothelial Progenitor Cells in BPD Risk Assessment?
Vivek Balasubramaniam and David A. Ingram
AJRCCM 2009 180: 488-490. [Full Text]  



This article has been cited by other articles:


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Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
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Am J Physiol Lung Cell Mol Physiol, December 1, 2009; 297(6): L1160 - L1169.
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Am. J. Respir. Crit. Care Med.Home page
V. Balasubramaniam and D. A. Ingram
Endothelial Progenitors in the Risk of Developing Bronchopulmonary Dysplasia: Can We Include Endothelial Progenitor Cells in BPD Risk Assessment?
Am. J. Respir. Crit. Care Med., September 15, 2009; 180(6): 488 - 490.
[Full Text] [PDF]




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