MiR-26b suppresses the development of stanford type a aortic dissection by regulating HMGA2 and TGF-β/smad3 signaling pathway

Abstract

Purpose: Stanford type A aortic dissection (TAAD) is one of the most dangerous cardiovascular diseases. MicroRNAs (miRNAs) have been considered as potential therapeutic targets for TAAD. In this present study, we aimed to investigate the functional role and regulatory mechanism of miR-26b in TAAD development. Materials and Methods: MiR-26b mRNA expression was detected by real-time polymerase chain reaction (RT-PCR) and protein levels were measured by Western blot. Verifying the direct target of miR-26b was used by dual luciferase assay, RT-PCR, and Western blot. Cell Counting Kit-8 (CCK-8) and TUNEL staining assays were applied for detecting rat aortic vascular smooth muscle cells (VSMCs) viability and apoptosis, respectively. Results: We found that miR-26b was under-expressed in TAAD patients and closely associated with the poor prognosis of TAAD patients. Re-expression of miR-26b facilitated while knockdown of miR-26b inhibited VSMC proliferation. However, miR-26b showed the opposite effect on cell apoptosis. More importantly, high-mobility group AT-hook 2 (HMGA2) was verified as the direct target of miR-26b. Furthermore, transforming growth factor beta (TGF-β)/Smad3 signaling pathway was involved in the development of TAAD modulated by miR-26b. Conclusion: miR-26b impeded TAAD development by regulating HMGA2 and TGF-β/ Smad3 signaling pathway, which provided a potential biomarker for TAAD treatment.