Long noncoding RNA myocardial infarction‑associated transcript is associated with the microRNA‑150‑5p/P300 pathway in cardiac hypertrophy

Abstract

In numerous diseases, abnormal expression of myocardial infarction-associated transcript (MIAT) has been reported to be involved in cell proliferation, apoptosis and migration. However, whether this long non-coding RNA MIAT has a regulatory effect on heart hypertrophy requires further investigation. To this end, the present study evaluated MIAT in hypertrophic cardiomyocytes in vitro and in vivo. Neonatal rat ventricular myocytes (NRVMs) were induced by isoproterenol (ISO) to create a cell hypertrophy model, and mice were intraperitoneally injected with ISO to establish an animal model. Echocardiography, immunofluorescence staining, western blot analysis, RNA isolation and reverse transcription-polymerase chain reaction were applied to test the involvement of MIAT in cardiac hypertrophy. The results revealed that MIAT was upregulated under ISO stimulation at the mRNA level both in vivo and in vitro. Silencing of MIAT resulted in decreased expression levels of atrial natriuretic peptide and brain natriuretic peptide in ISO-treated NRVM cardiomyocytes, confirming the connection between MIAT and hypertrophy. Furthermore, MIAT small interfering RNA significantly increased microRNA (miR)-150 and decreased P300 expression in NRVMs. In conclusion, the MIAT/miR-150-5p axis targets P300 as a positive regulator of cardiomyocyte hypertrophy.

Long non‐coding RNA small nucleolar RNA host gene 7 facilitates cardiac hypertrophy via stabilization of SDA1 domain containing 1 mRNA

“…lncRNAs are known to be a cluster of transcripts possessing little or no protein coding potential . Increasing research works have demonstrated the significant involvement of lncRNAs in human cancers and diseases, including in cardiac hypertrophy . SNHG7 is identified to bear oncogenic potential in multiple cancers .…”

“…9 Increasing research works have demonstrated the significant involvement of lncRNAs in human cancers and diseases, 1011-14 including in cardiac hypertrophy. [15][16][17][18] SNHG7 is identified to bear oncogenic potential in multiple cancers. [19][20][21] Nevertheless, its role in other diseases, such as cardiac hypertrophy, remains unknown.…”

“…Notably, the regulatory roles of lncRNAs have been increasingly revealed in cardiac hypertrophy. [15][16][17][18] Small nucleolar RNA host gene 7 (SNHG7) has been validated as an oncogene in a number of studies, regulating tumor progression and metastasis in various cancers such as bladder cancer, 19 colorectal cancer, 20 and lung cancer. 21 However, its involvement in cardiac hypertrophy remains unexplored.…”

Expedition to the missing link: Long noncoding RNAs in cardiovascular diseases

“…Zhu et al [36] found that MIAT regulates cardiac hypertrophy via sponging miR-150, a miRNA exhibiting antihypertrophic effects on cardiomyocyte. P300 was then determined to be the downstream effector of this MIAT-miR150 axis in promoting cardiac hypertrophy [37]. Additional studies by Li et al [38] showed that MIAT contributes to cardiac hypertrophy also by influencing the miR-93/TLR4 axis.…”

Regulation of Long Non-coding RNAs and MicroRNAs in Heart Disease: Insight Into Mechanisms and Therapeutic Approaches

“…Consistent with its hypertrophic effects, silencing MIAT results in a decreased expression of atrial natriuretic peptide and brain natriuretic peptide in ISO-treated NRVM cardiomyocytes. Under ISO treatment, MIAT acts by increasing P3000 expression levels via downregulation of miR-150p, resulting in cellular hypertrophy (Li et al, 2018c). MIAT has also been shown to promote the progression of AngII and isoproterenol induced cell hypertrophy in vitro by targeting miR-150 (Zhu et al, 2016).…”