Introduction. Failure of the vascular pulmonary remodeling at birth often manifests as pulmonary hypertension (PHT) and is\nassociated with a variety of neonatal lung disorders including a uniformly fatal developmental disorder known as alveolar capillary\ndysplasia with misalignment of pulmonary veins (ACD/MPV). Serumserotonin regulation has been linked to pulmonary vascular\nfunction and disease, and serotonin transporter (SERT) is thought to be one of the key regulators in these processes.We sought to\nfind evidence of a role that SERT plays in the neonatal respiratory adaptation process and in the pathomechanism of ACD/MPV.\nMethods.We used histology and immunohistochemistry to determine the timetable of SERT protein expression in normal human\nfetal and postnatal lungs and in cases of newborn and childhood PHT of varied etiology. In addition, we tested for a SERT gene\npromoter defect in ACD/MPV patients. Results.We found that SERT protein expression begins at 30 weeks of gestation, increases\nto term, and stays high postnatally. ACD/MPV patients had diminished SERT expression without SERT promoter alteration.\nConclusion. We concluded that SERT/serotonin pathway is crucial in the process of pulmonary vascular remodeling/adaptation\nat birth and plays a key role in the pathobiology of ACD/MPV.
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