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The present study analyzed gene expression arrays to identify differentially-expressed genes (DEGs) between mycophenolate mofetil (MMF)‑treated and placebo‑treated patients with symptomatic carotid artery stenosis (SCAS). In addition, the key genes involved in the pharmacology of MMF treatment in patients with SCAS were identified. The gene expression dataset was obtained from a Gene Expression Omnibus database, which included 9 MMF‑treated and 11 placebo‑treated samples. The DEGs were identified between MMF and placebo groups using R software. Furthermore, a protein‑protein interaction (PPI) network of the identified DEGS was constructed. The Database for Annotation, Visualization and Integrated Discovery was used to perform Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of the 19 most significant DEGs. A total of 210 DEGs between the MMF and placebo groups were screened and their PPI was constructed. GO function analysis revealed that the 19 DEGs were predominantly involved in the tyrosine phosphorylation of signal transducer and activator of transcription‑5 protein, which is closely associated with the activation of T cells. The KEGG pathway analysis suggested that the main metabolic pathways of the 19 DEGs were associated with the pharmacological functioning of MMF in activated T cells. In conclusion, the present study identified numerous key DEGs associated with SCAS, and the results suggested that v‑kit Hardy‑Zuckerman 4 feline sarcoma viral oncogene homolog and apelin may serve important roles in the MMF treatment of SCAS.

BACKGROUND Specific T cell phenotype has been reported to potentially contribute to the development of angiotensin II (Ang II)-induced several vascular disorders. Type 2 diabetes mellitus (T2DM) is intimately associated with cardiovascular disease. The present study aimed to investigate the relationship between T cell phenotypes and Ang II in T2DM patients combined with carotid atherosclerosis (CA). MATERIAL AND METHODS This study was performed on 50 patients with T2DM in our hospital. Based on the presence of CA, they were divided into CA group (presence of CA, n=30) or T2DM group (absence of CA, n=20). Additionally, 10 healthy participants were selected as controls. Basic characteristics of all participants were collected and recorded. Peripheral blood mononuclear cells (PBMCs) isolated from patients and controls with or without Ang II and Ang II receptor blocker (ARB) treatment were used to detect Th1, Th2, and Th17 cell proportions, mRNA levels of T-bet, GATA3, and RORγt as well as the expression of IFN-γ, IL-4, and IL-17 by flow cytometry, ELISA, and Real-Time PCR. RESULTS Ang II levels were notably higher in patients in the CA group than those in the T2DM and control group (p

To explore the expression and role of Caveolin-1 in the angiogenesis of cerebral arteriovenous malformation (AVM).A total of 55 fresh AVM samples at Affiliated Hospital, Inner Mongolia Medical University and Beijing Tiantan Hospital from August 2013 to May 2014 were collected to test the expressions of Caveolin-1, vascular endothelial growth factor (VEGF), vascular endothelial growth factor-receptor 2 (VEGF-R2) and endothelial nitric oxide synthase (eNOS) by immunohistochemistry and Western blot. And the relationship between the expressions of Caveolin-1 and VEGF, VEGF-R2 and eNOS was analysed.The expression rates of Caveolin-1, VEGF, VEGF-R2 and eNOS in human AVM were 100%, 87.27%, 76.36% and 85.45%. And the values were significantly higher than those in normal superficial temporal artery. Western blot showed that the expressions of Caveolin-1, VEGF, VEGF-R2 and eNOS in hemorrahge AVM were higher than those in non-hemorrahge counterpart (P0.05). The expressions of Caveolin-1, VEGF, VEGF-R2 and eNOS were consistent.Caveolin-1 plays a positive regulatory role in the angiogenesis of AVM through the PI3K/Akt signaling pathway. In cerebral AVM, Caveolin-1 plays an important role in occurrence, progression, hemorrahge and degradation of brain AVM.