Evaluation of mediators of fibrosis and angiogenesis in the blood serum of premature infants with bronchopulmonary dysplasia

In premature birth and postpartum damage to the developing lung, processes of formation pulmonary vessels alveoli are disrupted, leading bronchopulmonary dysplasia (BPD). BPD is a multifactorial disease pathogenesis lung tissue still not fully understood. Studies angiogenesis biomarkers can be informative for assessing development BPD. this study we examined blood serum 65 infants aged 6 180 days life; gestational age at was 23-33 weeks, body weight 480-1840 g, APGAR score 5-6. All children in early neonatal period had respiratory distress syndrome, then 46 formed 19 did form dysplasia. The concentration factors fibrosis determined by ELISA. There were no differences levels angiopoietins 1 2, vascular endothelial growth factor VEGF-D, transforming beta TGF-β, thrombospondin-1. We observed tendency increasing level VEGF-A, which key regulator maturation; regard as favorable sign formation. found tendencies increase adhesion molecule platelet cells PECAM-1, interleukin 8 connective CTGF. CTGF expression enhanced artificial ventilation exposure high oxygen concentrations. consider an unfavorable change, since binding VEGF inhibits VEGF-induced angiogenesis. with BPD, decrease derived PDGF-BB, median 3180 pg/mL versus 4782 without (p = 0.024). PDGF important regeneration plays role vessels. assume decreasing lead violation alveolarization necessary structure healthy lungs. will help better understand