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• W2007991523 abstract "Heterozygous ATP-binding-cassette subfamily A member 3 (ABCA3) mutations are associated with neonatal respiratory complications. In an adult murine model, we investigated whether Abca3 haploinsufficiency is a predisposing factor for lung injury induced by hyperoxia or mechanical ventilation. Abca3 haploinsufficient (Abca3+/−) and wild-type (WT) mice were prospectively randomized to 25 min of ventilation or 72 h of hyperoxia or left unchallenged in air. As compared with WT mice, unchallenged Abca3+/− mice had significantly decreased lung phosphatidylcholine (PC) and phosphatidylglycerol (PG) levels (P < 0.02) and decreased lung compliance (P < 0.05). When ventilated for 25 min, Abca3+/− mice demonstrated a significantly greater increase in bronchoalveolar lavage (BAL) interleukins (P ≤ 0.01) and lung wet to dry ratio (P < 0.005). Hyperoxia resulted in increased compliance (P < 0.05) and total lung capacity (TLC) (P = 0.01) only in the Abca3+/− mice, consistent with enlarged alveolar spaces. The ratio of PC to PG in BAL—relevant for surfactant dysfunction—was significantly elevated by oxygen exposure, with the greatest increase in Abca3+/− mice. In a murine model, Abca3 haploinsufficiency results in an altered biochemical and lung mechanical phenotype, as well as a greater lung injury induced by hyperoxia or mechanical ventilation. The inability to maintain a normal PC/PG ratio appears to play a key role." @default.
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• W2007991523 date "2013-07-23" @default.
• W2007991523 modified "2023-10-17" @default.
• W2007991523 title "Abca3 haploinsufficiency is a risk factor for lung injury induced by hyperoxia or mechanical ventilation in a murine model" @default.
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• W2007991523 doi "https://doi.org/10.1038/pr.2013.127" @default.
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