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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Activin Receptors, Type II, Activins, Animals, Animals, Newborn, Bronchopulmonary Dysplasia, Follistatin, Growth Disorders, Hyperoxia, Immunoglobulin Fc Fragments, Lung, Matrix Metalloproteinase 9, Mice, Mice, Inbred C57BL, Neutrophil Infiltration, Phosphorylation, Recombinant Fusion Proteins, Smad3 Protein.
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Does activin A contribute to the development of hyperoxia-induced lung injury in neonatal mice? Context: Bronchopulmonary dysplasia (BPD) is one of the leading causes of morbidity and mortality in babies born prematurely, yet there is no curative treatment. In recent years, a number of inhibitors against TGFβ signaling have been tested for their potential to prevent neonatal injury associated with hyperoxia, which is a contributing factor of BPD. In this study, we assessed the contribution of activin A-a member of the TGFβ superfamily-to the development of hyperoxia-induced lung injury in neonatal mice. We placed newborn C57Bl6 mouse pups in continuous hyperoxia (85% O2) to mimic many aspects of BPD including alveolar simplification and pulmonary inflammation. The pups were administered activin A receptor type IIB-Fc antagonist (ActRIIB-Fc) at 5 mg/kg or follistatin at 0.1 mg/kg on postnatal days 4, 7, 10, and 13. Treatment with ActRIIB-Fc and follistatin protected against hyperoxia-induced growth retardation. ActRIIB-Fc also reduced pulmonary leukocyte infiltration, normalized tissue: airspace ratio and increased septal crest density. These findings were associated with reduced phosphorylation of Smad3 and decreased matrix metalloproteinase (MMP)-9 activity.
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This study suggests that activin A signaling may contribute to the pathology of bronchopulmonary dysplasia. Final Decision: yes