BackgroundFibroblast growth factors (FGF) are essential key players during embryonic development. Through their specific cognate receptors (FGFR) they activate intracellular cascades, finely regulated by modulators such as Sprouty. Several FGF ligands (FGF1, 2, 7, 9, 10 and 18) signaling through the four known FGFRs, have been implicated in lung morphogenesis. Although much is known about mammalian lung, so far, the avian model has not been explored for lung studies.Methodology/Principal FindingsIn this study we provide the first description of fgf10, fgfr1-4 and spry2 expression patterns in early stages of chick lung development by in situ hybridization and observe that they are expressed similarly to their mammalian counterparts. Furthermore, aiming to determine a role for FGF signaling in chick lung development, in vitro FGFR inhibition studies were performed. Lung explants treated with an FGF receptor antagonist (SU5402) presented an impairment of secondary branch formation after 48 h of culture; moreover, abnormal lung growth with a cystic appearance of secondary bronchi and reduction of the mesenchymal tissue was observed. Branching and morphometric analysis of lung explants confirmed that FGFR inhibition impaired branching morphogenesis and induced a significant reduction of the mesenchyme.Conclusions/SignificanceThis work demonstrates that FGFRs are essential for the epithelial-mesenchymal interactions that determine epithelial branching and mesenchymal growth and validate the avian embryo as a good model for pulmonary studies, namely to explore the FGF pathway as a therapeutic target.
Fetal primary hydrothorax is a rare congenital anomaly with an estimated incidence of 1:10.000–15.000 pregnancies, with an unpredictable clinical course, ranging from spontaneous resolution to fetal death. We present a case of a unilateral fetal pleural effusion identified at 35th gestational week. A 37 year-old woman (G2P1) presented to our routine term pregnancy evaluation. The pregnancy had been otherwise uneventful. At ecographic evaluation a large anechogenic fluid collection was identified in the right fetal hemithorax, with atelectasis of right lung, displacing the heart and mediastinal structures to the contralateral hemithorax. Hydramnios was also identified. No other structural abnormalities were detected, as no signs of hydrops. Fetal biometry was compatible with gestational age. Fetal ecochardiogram was structurally and functionally normal. Doppler evaluation of the peak systolic velocity in the middle cerebral artery was normal. Screening for congenital infections was negative. Complete blood cell count, blood type and antibody screening rulled-out immune hydrops. Karyotype analysis was not performed as family decision. Serial ecographic re-evaluations showed a progressive volume decrease and at the 38th week there was total resolution of the effusion. A C-section was performed at the 39th week. A live female infant was born weighing 3205 g, with no need of ventilatory support. One year post-partum follow-up evaluation confirmed the child was healthy. Spontaneous regression has been reported to occur in 9–22% of primary fetal hydrothoraxes, but the features predicting a better prognosis remain difficult to define. Unilateral effusion, spontaneous resolution and absence of hydrops at the age of diagnosis seem to be indicators of better outcome.
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