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Background: Coronary artery disease (CAD) is a common cardiovascular disease that has attracted attention worldwide due to its high morbidity and mortality. Recent studies have shown that abnormal microRNA (miRNA) expression is effective in CAD diagnoses and processes. However, the potential relationship between miRNAs and CAD remains unclear. Methods: Microarray datasets GSE105449 and GSE28858 were downloaded directly from the Gene Expression Omnibus (GEO) to identify miRNAs involved in CAD. Target gene prediction and enrichment analyses were performed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Results: There were nine differentially expressed miRNAs in CAD patients compared to the controls. A total of 352 genes were predicted and subjected to GO analysis, which showed that differentially expressed genes (DEGs) were mainly associated with axon guidance, neuron projection guidance, neuron-to-neuron synapses, and postsynaptic density. According to the KEGG pathway analysis, the most enriched pathways were those involved in transcriptional misregulation in cancer, growth hormone synthesis, secretion and action, endocrine resistance, axon guidance, and Cushing syndrome. Pathway analysis was mainly involved in the HIPPO and prion disease signaling pathways. Furthermore, a competing endogenous RNA (ceRNA) interaction network centered on miR-22-3p revealed eight related transcription factors in the cardiovascular system. The receiver operating characteristic (ROC) curve analysis suggested that miR-22-3p may be a better CAD predictor. Conclusion: The results indicate that miR-22-3p may function in pathophysiological CAD processes. Our study potentiates miR-22-3p as a specific biomarker for diagnosing CAD.
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Arteriosclerosis poses a significant risk to human health and involves the thickening and hardening of the walls of arteries. Accumulated evidence demonstrates that aberrant proliferation of vascular smooth muscle cells (VSMCs) accounts for the onset and progression of arteriosclerosis. Suppression of their proliferation has been demonstrated to be an effective anti-arteriosclerosis strategy. Long non-coding RNAs (lncRNAs) have recently been observed to be implicated in the proliferation of VSMCs and arteriosclerosis. In this study, we observed that oleanolic acid (OA), a natural compound from plants, inhibited the proliferation of VSMCs. The expression of lincRNA-p21, an arteriosclerosis-associated lncRNA, was demonstrated to be elevated by OA treatment. Suppression of lincRNA-p21 rescued the effect of OA on the proliferation of VSMCs. Collectively, targeting lncRNA is a promising strategy for arteriosclerosis prevention and treatment, and OA ameliorates arteriosclerosis by increasing lncRNA levels.
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In some GWAs studies, GALNT2 and APOE polymorphisms have been identified to be related to alterations of plasma or serum HDL-C and TG concentrations. The purpose of our study is to assess the contribution of GALNT2 rs4846914, APOE rs429358, rs7412, rs405509 variants, and several environmental factors to the development of hypertension disease in the China Han population. A hospital-based case-control study was conducted. Cases were hypertension (n=211) and controls were normal participants (n=434). The AA, AG, and GG genotype frequencies of GALNT2 rs4846914 were 22.8%, 43.1%, and 34.1% in hypertension subjects, and 35.3%, 44.2%, and 20.5% in controls (P<0.05), respectively. The OR of the AG genotype adjusted for all risk factors compared to the AA genotype was 1.61 (95%CI: 1.02 to 2.56) and to the GG genotype 2.67 (95%CI: 1.59 to 4.488). There was no significant difference between the APOE rs429358, rs7412, and rs405509 genotype frequencies in hypertension and control subjects. The present work indicates that SNP rs4846914 in GALNT2 gene is related to an increased risk of hypertension in China Han population, but the APOE gene is not.
