Lung transcriptomes of wild type, ß-arrestin 1 -/-, and ß-arrestin 2 -/- mice exposed to normoxia or chronic hypoxia

We found that ß-arrestin 1 -/- mice were more sensitive to hypoxia-induced pulmonary arterial hypertension with increased right ventricle hypertrophy and higher right ventricle systolic pressure, while ß-arrestin 2 -/- mice developed right ventricle hypertrophy comparable to wild type mice. Moreover, ß-arrestin 1 -/- mice had worse right ventricle function than wild type mice in response to chronic hypoxia, whereas ß-arrestin 2 -/- mice relatively preserved right ventricle function compared to wild type mice. To investigate the molecular mechanisms responsible for the worse PAH in ß-arrestin 1 -/- mice, we performed lung transcriptome analysis of wild type, ß-arrestin 1 -/-, and ß-arrestin 2 -/- mice using high-throughput RNA-seq. Overall design: Deep sequencing of lung transcriptomes from wild type, ß-arrestin 1 -/-, and ß-arrestin 2 -/- mice exposed to normoxia or chronic hypoxia in triplicate.