We hypothesize that the PSC stage-specific markers of endogenous embryonic antigen-1 (SSEA-1) and an enzyme, α1,3-fucosyltransferase IX (FUT9) plays an important role in reducing inflammation and restoring lung structure on a trial studying the expression BPD.We SSEA-1, and FUT9 enzyme, in wild-type (WT) C57BL / 6 mice, in room air and hyperoxia.
Effect of intraperitoneal administration of recombinant human FUT9 (rhFUT9) on lung airway and parenchymal inflammation, alveolarization, and apoptosis evaluated.On exposure to hyperoxia, SSEA-1 was significantly decreased at postnatal day 14 in BPD mice exposed to hyperoxia, surface staining accompanied by a decrease FUT9 , BPD and respiratory distress syndrome (RDS) in human lung showed decreased expression of SSEA-1 compared to control their term. Importantly, the intraperitoneal administration of FUT9 the BPD model of neonatal rats resulted in a significant reduction in the airways of the lung (but not the lung parenchyma) inflammation, alveolar-capillary leak, alveolar simplification, and cell death in BPD mice.
An hyperoxia-exposed important role of endogenous PSC marker SSEA-1 and enzyme FUT9 shown, indicating the beginning of a systemic intervention with FUT9 as a potential therapeutic option for BPD.Administration of rhFUT9, enzymes endogenous stem cell marker SSEA-1, reducing breath pulmonary (lung parenchyma but not) inflammation , alveolar-capillary leak and cell death in mice model.SSEA BPD-1 was reported for the first time in a model of experimental BPD and RDS BPD.rhFUT9 treatment ameliorates human and hyperoxia-induced lung injury in BPD developmentally appropriate mice results model.
Our have translational potential as a therapeutic modality for BPD in the lungs develop.
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