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Reduction In MiR-133a/b Expression in Lungs During Hyperoxia Leads to the Development of Pulmonary Hypertension in Neonatal Mice
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A6969 - Reduction In MiR-133a/b Expression in Lungs During Hyperoxia Leads to the Development of Pulmonary Hypertension in Neonatal Mice
Author Block: T. Chen; Pediatrics, UIC, Chicago, IL, United States.
Rationale: We have found that in a hyperoxia-induced bronchopulmonary dysplasia (BPD) and pulmonary hypertension (PH) model in neonatal mice, miR-133a/b expression was significantly decreased in the lungs after exposure to hyperoxia for 2 weeks. We also found that miR-133a/b suppressed pulmonary arterial smooth muscle cell (PASMC) proliferation and induced the expression of contractile proteins in PASMC, suggesting a protective role of miR-133a/b in the development of PH. In this study, we investigated whether miR-133a/b can ameliorate the development of PH in hyperoxia-induced BPD and PH in neonatal mice in-vivo. Methods: We exposed neonatal mice (1-3 d old) to hyperoxia (75% O2) for 2 weeks and then maintained them in room air for 4 more weeks. MiR-133a/b mimics were given to these mice via retro-orbital injections, from the beginning of room air exposure post-hyperoxia, once a week for four weeks. Negative control miRNA mimics (Ambion) were injected as the control for the experiment. At the end of the 4-week room air period, we measured right ventricular systolic pressure (RVSP), RV hypertrophy [RV/(LV+S) ratio], and pulmonary arterial wall thickness in these mice. Results: We found that injection of miR-133a/b mimics suppressed the increase in RVSP in neonatal mice exposed to hyperoxia. Conclusions: Our results suggest that miR-133a/b may play a therapeutic role in the treatment of PH associated with hyperoxia-induced BPD.
Author Block: T. Chen; Pediatrics, UIC, Chicago, IL, United States.
Rationale: We have found that in a hyperoxia-induced bronchopulmonary dysplasia (BPD) and pulmonary hypertension (PH) model in neonatal mice, miR-133a/b expression was significantly decreased in the lungs after exposure to hyperoxia for 2 weeks. We also found that miR-133a/b suppressed pulmonary arterial smooth muscle cell (PASMC) proliferation and induced the expression of contractile proteins in PASMC, suggesting a protective role of miR-133a/b in the development of PH. In this study, we investigated whether miR-133a/b can ameliorate the development of PH in hyperoxia-induced BPD and PH in neonatal mice in-vivo. Methods: We exposed neonatal mice (1-3 d old) to hyperoxia (75% O2) for 2 weeks and then maintained them in room air for 4 more weeks. MiR-133a/b mimics were given to these mice via retro-orbital injections, from the beginning of room air exposure post-hyperoxia, once a week for four weeks. Negative control miRNA mimics (Ambion) were injected as the control for the experiment. At the end of the 4-week room air period, we measured right ventricular systolic pressure (RVSP), RV hypertrophy [RV/(LV+S) ratio], and pulmonary arterial wall thickness in these mice. Results: We found that injection of miR-133a/b mimics suppressed the increase in RVSP in neonatal mice exposed to hyperoxia. Conclusions: Our results suggest that miR-133a/b may play a therapeutic role in the treatment of PH associated with hyperoxia-induced BPD.
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