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MiR-126 delays the formation of aortic dissections in rats through interaction with MAPK signaling pathway
Abstract
Purpose: To investigate the impact of microRNA (miR)-126 on aortic dissections using rat aortic smooth muscle cells (RASMCs).
Methods: The cell model of AD (MA-RASMCs) was established by co-culturing RASMCs with angiotensin II (Ang II). The cells were then transfected with miR-126 control and miR-126 mimic. Transfection efficiency was assessed using quantitative reverse transcription- polymerase chain reaction (qRT-PCR). The proliferative and migratory potentials of the cells were determined, as well as the expression levels of related proteins, i.e., Ras, matrix metalloproteinase-2 (MMP2), tissue inhibitor of metalloproteinase 1 (TIMP1), phosphorylated MAPK (p-MAPK), and phosphorylated ERK (p-ERK).
Results: Compared to RASMCs, MA-RASMCs exhibited enhanced proliferation and migration, and decreased miR-126 expression (p < 0.05). MA-RASMCs transfected with miR-126 mimic, reduced its proliferative potential, increased miR-126 expression, and lowered the expression levels of Ras, MMP2, p-MAPK, and p-ERK (p < 0.05). Furthermore, the transfected cells had higher expression levels of TIMP1 (p < 0.05).
Conclusion: MicroRNA-126 inhibits the proliferation and migration of RASMCs by modulating MAPK/ERK pathway, thereby delaying the formation of aortic dissections. Thus miR-126 is a potential therapeutic target for aortic dissections.
