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LncRNA MIAT stimulates oxidative stress in the hypoxic pulmonary hypertension model by sponging miR-29a-5p and inhibiting Nrf2 pathway.

OBJECTIVE
To elucidate the potential biological functions of long non-coding RNA (lncRNA) MIAT in the development of hypoxic pulmonary hypertension (HPH) and the underlying mechanism.


MATERIALS AND METHODS
Twenty Sprague Dawley (SD) rats were randomly assigned into normoxia group (n=10) and hypoxia group (n=10), respectively. In vivo HPH model in rats was established by hypoxic induction. Expression levels of MIAT and miR-29a-5p in rats were detected. Meanwhile, hemodynamic indicators in rats were examined. In vitro HPH model was conducted in hypoxia-induced HPAECs. The interaction between MIAT and miR-29a-5p was assessed by Dual-Luciferase reporter assay. Moreover, their regulatory effects on viability, migratory ability, oxidative stress, and the Nrf2 pathway in hypoxia-induced HPAECs were examined.


RESULTS
MIAT was upregulated in both in vivo and in vitro HPH models, while miR-29a-5p was downregulated. Knockdown of MIAT suppressed viability, migratory ability, and oxidative stress in hypoxia-induced HPAECs. MiR-29a-5p was the target gene binding MIAT, and silence of miR-29a-5p partially relieved the inhibitory effects of MIAT on the above regulations in HPAECs.


CONCLUSIONS
MIAT promotes proliferative and migratory abilities, as well as oxidative stress in hypoxia-induced HPAECs by targeting miR-29a-5p, thus aggravating the development of HPH.