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Abstract
Restenosis is the main restriction on the long-term efficacy of percutaneous transluminal angioplasty (PTA) therapy for peripheral artery disease (PAD). Interventions to prevent restenosis are poor, and the exact mechanism is unclear. Here, we aimed to elucidate the role of GRIA2 in the restenosis process post-PTA in lower extremity arteries. We searched the differentially expressed genes (DEGs) between atherosclerotic and restenotic artery plaques in the Gene Expression Omnibus (GEO), and five DEGs were identified. Combined with Gene Ontology (GO) enrichment analysis, GRIA2 was significantly correlated with the restenosis process. Tissue samples were used to examine GRIA2 expression by immunofluorescence staining of atherosclerotic and restenotic artery plaques. The regulation of GRIA2 in vascular smooth muscle cells (VSMCs) was confirmed by lentiviral transfection. Overexpression of GRIA2 promoted the proliferation and migration of VSMCs. Using Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis and protein–protein interaction (PPI) network, a strong connection between ENPP3 and GRIA2 was discovered. In vitro results showed that the high expression of GRIA2 in VSMCs enhanced the expression of ENPP3, while downregulation of GRIA2 downregulated ENPP3. GRIA2 is highly differentially expressed in restenotic arterial plaques, promoting the proliferation and migration of VSMCs through upregulation of ENPP3. These discoveries will help us to obtain a better understanding of restenosis in lower extremity arteries.
Highlights
Peripheral artery disease (PAD) affects approximately 15–20% of persons over 70 years of age (Criqui et al, 1985; Hiatt et al, 1995; Selvin and Erlinger, 2004), and chronic atherosclerotic ischemia of the lower extremities leads to a high amputation rate and mortality (Diehm et al, 2009; Zeller et al, 2009; Meves et al, 2010)
GSE23314 and GSE53274 were chosen, and through the analysis of the two datasets, we discovered significant differences in glutamate ionotropic receptor AMPA type subunit 2 (GRIA2) expression in restenosis and atherosclerosis tissues
GRIA2 levels in restenosis were confirmed to be highly expressed in vascular smooth muscle cells (VSMCs) in the intima
Summary
Peripheral artery disease (PAD) affects approximately 15–20% of persons over 70 years of age (Criqui et al, 1985; Hiatt et al, 1995; Selvin and Erlinger, 2004), and chronic atherosclerotic ischemia of the lower extremities leads to a high amputation rate and mortality (Diehm et al, 2009; Zeller et al, 2009; Meves et al, 2010). Despite the wide use of percutaneous transluminal angioplasty (PTA), due to its minimal invasiveness and effectiveness (Apelqvist et al, 2011), restenosis occurs in up to 70% of patients within 1 year (Liistro et al, 2013) and limits the GRIA2/ENPP3 Participates in Restenosis Post-PTA long-term efficacy. Restenosis has become the main obstacle to long-term efficacy post-PTA in lower extremity arteries. Elucidating the regulatory mechanism of restenosis post-PTA will aid in significantly improving PTA prognosis and the long-term patency rate of lower extremity arteries. Clarifying the mechanism of VSMCs migration and proliferation in restenosis may provide new research insights into the causes of restenosis, which may lead to treatment strategies that ameliorate the overall efficacy of PTA treatment
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