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The PPAR Gamma Agonist Rosiglitazone Protects Against Wnt Signaling In Hyperoxia‐Induced Neonatal Rat Lung Injury

Bronchopulmonary Dysplasia (BPD) is a consequence of abnormally repaired lung damage. Hyperoxia disrupts critical signaling pathways that support normal lung development. We characterized in vivo hyperoxia induced perturbations in lung morphology and Wnt and TGF‐β signaling in postnatal day (PND) 7 rat lung, and tested if the PPARγ agonist rosiglitazone (RGZ) prevents such perturbations. Newborn rats were grouped as normoxic, hyperoxic (95% O2), and hyperoxic/RGZ (3 mg/kg i.p. daily during 95% O2). PND7 lungs were analyzed by immunoblot, morphometry, and immunohistochemistry (IHC). Hyperoxia caused significant up‐regulation of Wnt signaling markers Lef1 and βcatenin, and TGFβ pathway markers pSMAD3 and SMAD7. The myogenic phenotype markers αSMA and calponin were also up‐regulated. There was significantly reduced alveolar septal thickness, radial alveolar count, but larger alveoli. PPARγ expression, however, was significantly down‐regulated. Hyperoxia‐induced changes were almost completely prevented by RGZ treatment. We demonstrate up‐regulation of Lef1, βcatenin, pSMAD3 and SMAD7 in neonatal rat lungs in hyperoxia. Hyperoxia‐induced simplified alveoli, a hallmark of BPD, along with altered molecular changes, strongly implicating these factors in hyperoxia‐induced lung injury. PPARγ agonists may effectively prevent BPD Grant Support‐NIH HL75405 & HL55268 & TRDRP 15IT‐0250 & 14RT‐0013.