LncRNA MIAT enhances cardiac hypertrophy partly through sponging miR-150.

OBJECTIVE: In this work, we aimed to study whether myocardial infarction associated transcript (MIAT) exerts a regulative effect on cardiac hypertrophy via acting as a miR-150 sponge.
MATERIALS AND METHODS: Cardiac hypertrophy was induced using Angiotensin II (Ang II). MIAT and miR-150 expression were quantified using qRT-PCR. Rat heart-derived H9c2 cells were used as the in vitro model. Cardiac hypertrophic features were assessed by quantifying cardiac hypertrophic genes and measurement of cell surface, protein synthesis and total protein content.
RESULTS: MIAT is significantly increased in Ang II induced cardiac hypertrophy in a mouse model and in H9c2 cells. MIAT siRNA substantially alleviated the Ang II induced upregulation of ANP, BNP and β-MHC in H9c2 cells and markedly attenuated the Ang II induced increase of the cell surface area and the protein synthesis. MIAT overexpression in H9c2 cells significantly reduced the miR-150 expression. MIAT inhibition also partly restored the miR-150 levels under Ang II treatment. MiR-150 overexpression could attenuate the Ang II induced upregulation of hypertrophic marker genes and suppress the Ang II induced hypertrophic phenotypes of the cells.
CONCLUSIONS: MIAT is significantly increased in Ang II induced cardiac hypertrophy and contributes to the pathological development. MIAT can suppress miR-150 expression in cardiomyocytes and miR-150 is a downstream effector of MIAT in the development of cardiac hypertrophy.