MIAT promotes proliferation and hinders apoptosis by modulating miR-181b/STAT3 axis in ox-LDL-induced atherosclerosis cell models.

BACKGROUND

Plenty of lncRNAs and microRNAs have been identified to be critical mediators in the progression of atherosclerosis (AS). Myocardial infarction-associated transcript (MIAT) were aberrantly high expressed and closely associated with the pathogenesis of AS. However, its molecular mechanism has not been well characterized.

METHODS

The expression patterns of MIAT and microRNA-181b (miR-181b) in clinical samples and cells were measured by RT-qPCR assays. Luciferase reporter assay and RIP assays were used to manifest the potential interaction between MIAT, miR-181b and signal transducer and activator of transcription 3 (STAT3). Cell Counting Kit-8 (CCK-8), Propidium Iodide (PI) staining, Terminal dexynucleotidyl transferase(TdT)-mediated dUTP nick end labeling (TUNEL) and western blot assays were carried out to detect cell proliferation, cell cycle distribution, apoptosis, and STAT3 protein level, respectively.

RESULTS

MIAT expression was up-regulated and miR-181b expression was down-regulated in AS patients serum and oxidized low-density lipoprotein (ox-LDL) induced AS cells model. MIAT facilitated cell proliferation, accelerated cell cycle progression and inhibited apoptosis in ox-LDL-induced AS cell lines, while this effect was partly reversed by miR-181b overexpression. Moreover, MIAT enhanced STAT3 expression through sequestering miR-181b as a molecular sponge. Furthermore, MiR-181b hindered cell growth, induced cell cycle arrest and promoted apoptosis by directly targeting STAT3.

CONCLUSION

MIAT performed as an induction factor of AS by regulating miR-181b/STAT3 axis in ox-LDL-induced AS cell lines, offering a new insight into the potential application of MIAT in AS treatment.