Fig. 6.
Ten-eleven translocation methylcytosine dioxygenase 2 (TET2)-mediated glucose-6-phosphate dehydrogenase (G6PD) inhibition-induced upregulation of molecular footprints and reversal of hypoxia-induced pulmonary hypertension (PH). G6PD inhibitor N-ethyl-N′-[(3β,5α)-17-oxoandrostan-3-yl]urea (NEOU; 1.5 mg·kg−1·day−1; sc): increased expression of lncPint, Bmpr1b, and Tet2 genes in lungs of wild-type (WT) mice, but not in TET2 global knockout (Tet2tm1.2Rao; Tet2−/−) mice (A–C); significantly reduced hypoxia-induced increase of right ventricle systolic pressure (RVSP) and right ventricle hypertrophy (RVH) (D and E); and increased cardiac index (CI) in WT mice, but not in Tet2tm1.2Rao (Tet2−/−) mice (F). Values are means ± SD; n = 5 in WT group (male 3 and female 2) and n = 4 in Tet2tm1.2Rao (male 2 and female 2). *P < 0.05 vs. normoxia and #P < 0.05 vs. control (ctrl).