Identification of Genes Differentially Expressed in Vascular Smooth Muscle Cells following Benzo[A]Pyrene Challenge: Implications for Chemical Atherogenesis

1998 ◽  
Vol 253 (3) ◽  
pp. 828-833 ◽  
Author(s):  
K.P. Lu ◽  
K.S. Ramos
2021 ◽  
Vol 12 ◽  
Author(s):  
Mi Zhou ◽  
Lixing Qi ◽  
Yongquan Gu

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.


2020 ◽  
Author(s):  
Jiangtian Tian ◽  
Yahong Fu ◽  
Qi Li ◽  
Ying Xu ◽  
Xiangwen Xi ◽  
...  

Abstract Background: Atherosclerosis is mediated by various factors and plays an important pathological foundation for cardiovascular and cerebrovascular diseases. Abnormal VSMC proliferation and migration have an essential role in atherosclerotic lesion formation. Circular RNAs have been widely detected in different species and are closely related to various diseases. However, the expression profiles and molecular regulatory mechanisms of circRNAs in VSMCs are still unknown. Methods: We used high-throughput RNA-seq as well as bioinformatics tools to systematically analyze circRNA expression profiles in samples from different VSMC phenotypes. PCR, Sanger sequencing, and qRT-PCR were performed for circRNA validation. Results: A total of 22191 circRNAs corresponding to 6273 genes (host genes) in the PS, NC or both groups, were detected, and 112 differentially expressed circRNAs were identified between the PS and NC groups, of which 59 were upregulated and 53 were downregulated. We selected 9 circRNAs for evaluation of specific head-to-tail splicing, and 10 differentially expressed circRNAs between the two groups for qRT-PCR validation. Gene Ontology and KEGG pathway enrichment analyses revealed that the parental genes of the circRNAs mainly participated in cardiac myofibril assembly and positive regulation of DNA-templated transcription, indicating that they might be involved in cardiovascular diseases. Finally, we constructed a circRNA-miRNA network based on the dysregulated circRNAs and VSMC-related miRNAs. Conclusion: The current study is the first to show the differential expression of circRNAs in PDGF-BB-induced vascular smooth muscle cells and may provide new ideas and targets for the prevention and therapy of vascular diseases.


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