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Objectives   To observe the effect of av β 3 single-stranded (ss) DNA on proliferation and migration of vascular smooth muscle cells (VSMCs) and its potential mechanism.Background   Percutaneous transluminal coronary angioplasty (PTCA) is currently the preferred method for the treatment of coronary heart disease. However, vascular restenosis still occurs after PTCA treatment, severely affecting the clinical efficacy of PTCA. Integrin av β 3, which is widely expressed on various cell surfaces, plays an important role in the proliferation and migration of VSMCs.Methods   In this experiment, we used systematic evolution of ligands by exponential enrichment (SELEX) to screen out av β 3 ssDNA, which has high affinity and specificity to the av β 3 protein. MTT, Transwell, and cell scratch assays were carried out to examine the effect of av β 3 ssDNA on the proliferation and migration of VSMCs. Flow cytometry was performed to detect apoptosis and cell cycle progression. The effect of av β 3 ssDNA on the Ras-phosphatidylinositol-4,5-bisphosphate 3-kinase/mitogen-activated protein kinase (PI3K/MAPK) signaling pathway was evaluated by quantitative reverse transcription polymerase chain reaction and western blot.Results   In the present study, we found that av β 3 ssDNA significantly decreased the expression of osteopontin, focal adhesion kinase, Ras, p-PI3K, and p-MAPK at both mRNA and protein levels ( P  < 0.05). Av β 3 ssDNA also inhibited VSMC proliferation and migration while promoting apoptosis ( P  < 0.05), as demonstrated by the upregulation of the proapoptotic proteins Bax and active caspase 3 ( P  < 0.05).Conclusions   The findings suggest that av β 3 ssDNA inhibited the proliferation and migration of VSMCs by suppressing the activation of Ras-PI3K/MAPK signaling.

Avβ3 Single-Stranded DNA Aptamer Attenuates Vascular Smooth Muscle Cell Proliferation and Migration via Ras-PI3K/MAPK Pathway