Figures & data
Figure 1. Omentin-1 attenuated hypoxia-induced PAH. SD rats were exposed to a low-oxygen chamber (10% O2 with balanced N2) or normal air with saline or omentin-1 (18 μg/kg/day) treatment for 4 weeks. (a) omentin-1 levels were measured by ELISA kit. (b and c) right ventricular systolic pressure (RVSP) and right ventricular hypertrophy index (RVHI) in control (vehicle) and omentin-1 treated rats exposed to normoxia or hypoxia. (D1 and D2) Representative images of arteries and quantification of ratio of vascular medial thickness to total vessel size were shown. Data are expressed as the means ± SD (n=5/group). *p <.05 vs others. N+V, normoxia+Vehicle; N+O, normoxia+Omentin-1; H+V, hypoxia+Vehicle; H+O, hypoxia+ omentin-1.
Figure 2. Omentin-1 improved endothelial function of pulmonary artery in rats exposed to hypoxia. SD rats were exposed to a low-oxygen chamber (10% O2 with balanced N2) or normal air with saline or omentin-1 (18 μg/kg/day) treatment for 4 weeks. (a-c) ach-induced relaxation, ach-induced relaxation with L-NAME and SNP-induced relaxation in pulmonary artery from the rats exposed to hypoxia or normal air. Data are expressed as the means ± SD (n=5/group). *p <.05 vs others. N+V, normoxia+Vehicle; N+O, normoxia+Omentin-1; H+V, hypoxia+Vehicle; H+O, hypoxia+ omentin-1.
Figure 3. Omentin-1 increased NO production in pulmonary-artery rings from rats exposed to hypoxia. SD rats were exposed to a low-oxygen chamber (10% O2 with balanced N2) or normal air with saline or omentin-1 (18 μg/kg/day) treatment for 4 weeks. (a and b) NO metabolites in endothelium-intact pulmonary arteries and phosphorylation and expression of eNOS at Ser1177 in pulmonary artery from the rats exposed to hypoxia or normal air. Data are expressed as the means ± SD (n=5/group). *p <.05 vs others. N+V, normoxia+Vehicle; N+O, normoxia+Omentin-1; H+V, hypoxia+Vehicle; H+O, hypoxia+ omentin-1.
Figure 4. Omentin-1 attenuated ER stress in pulmonary-artery rings from rats exposed to hypoxia. SD rats were exposed to a low-oxygen chamber (10% O2 with balanced N2) or normal air with saline or omentin-1 (18 μg/kg/day) treatment for 4 weeks. (a-c) the expressions of ER stress markers, such as p-PERK and ATF-6, and NADPH oxidase activity in lysates of pulmonary artery from the rats exposed to hypoxia or normal air. Data are expressed as the means ± SD (n=5/group). *p <.05 vs others. N+V, normoxia+Vehicle; N+O, normoxia+Omentin-1; H+V, hypoxia+Vehicle; H+O, hypoxia+ omentin-1.
Figure 5. Omentin-1 alleviated ER stress dependent on AMPKα signaling in rats exposed to hypoxia. SD rats were exposed to a low-oxygen chamber (10% O2 with balanced N2) or normal air for 4 weeks. (a-d) phosphorylation and expression of AMPKα, expression of ATF-6, phosphorylation and expression of eNOS at Ser1177 and ach-induced relaxation in pulmonary artery from the rats incubated with omentin-1 alone or in the presence of compound C, AMPK inhibitor (5 μmol/L) for 16 h. Data are expressed as the means ± SD (n=5/group). *p <.05 vs N+V; #p <.05 vs H+O. N+V, normoxia+Vehicle; H+V, hypoxia+Vehicle; H+O, hypoxia+ omentin-1; H+O+C, hypoxia+ omentin-1+ compound C.
