Background. This current study applied bioinformatics analysis to reveal the crosstalk between venous thromboembolism (VTE) and periodontitis, as well as the potential role of immune-related genes in this context. Methods. Expression data were downloaded from the GEO database. Blood samples from venous thromboembolism (VTE) were used (GSE19151), while for periodontal disease, we used gingival tissue samples (GSE10334, GSE16134, and GSE23586). After batch correction, we used “limma” packages of R language for differential expression analysis (
p
value < 0.05,
∣
logFC
∣
≥
0.5
). We used Venn diagrams to extract the differentially expressed genes common to VTE and periodontitis as potential crosstalk genes and applied functional enrichment analysis (GO biological process and KEGG pathway). The protein-protein interaction (PPI) network of crosstalk genes was constructed by Cytoscape software. The immune-related genes were downloaded from the literature. The Wilcoxon test was used to test the scores of immune infiltrating cells. The crosstalk genes were further screened by LASSO Logistic Regression. Results. For periodontitis, 427 case and 136 control samples, and for VTE, 70 case and 63 control samples were included. The obtained PPI network had 1879 nodes and 2257 edges. Moreover, 782 immune genes and 28 cell types were included in the analysis. Over 90% of immune cells had different expressions in VTE and periodontitis. We obtained 12 significant pathways corresponding to crosstalk genes. CD3D, CSF3R, and CXCR4 acted as an immune gene and a crosstalk gene. We obtained a total of 12 shared biomarker crosstalk genes. Among those 12 biomarker crosstalk genes, 4 were immune genes (LGALS1, LSP1, SAMSN1, and WIPF1). Conclusion. Four biomarker crosstalk genes between periodontitis and VTE were also immune genes, i.e., LGALS1, LSP1, SAMSN1, and WIPF1. The findings of the current study need further validation and are a basis for development of biomarkers.
Background. The role and expression level change in circ_TNPO1 (hsa_circ_0072951) in atherosclerosis (AS) and VSMC dysfunction remain unknown. In this study, we try to explore the effects of circ_TNPO1 on oxidized low-density lipoprotein (ox-LDL)-induced human vascular smooth muscle cell (VSMC) excessive proliferation and migration, and the potential molecular mechanism. Methods. Quantitative real-time polymerase chain reaction (RT-qPCR) and western blot experiment were used to detect the serum samples from AS patients and healthy controls. CCK-8, Transwell, and the dual-luciferase reporter gene assay were used to detect the cell biology. Results. In human AS serum and ox-LDL-induced VSMCs, circ_TNPO1 was increased, whereas miR-181b was decreased. Silencing circ_TNPO1 inhibited proliferation and migration activity and reduced protein expression of PCNA, Ki-67, MMP2, and E-cadherin and promoted N-cadherin protein expression in ox-LDL induced VSMCs. Remarkably, miR-181b knockdown or Notch1 overexpression could efficiently offset the proliferation and migration inhibiting effect of circ_TNPO1 knockdown in ox-LDL-induced VSMCs. Furthermore, a molecular mechanism study pointed out that circ_TNPO1 and Notch1 are direct-acting targets of miR-181b. Conclusions. In conclusion, our study indicated that circ_TNPO1 promotes the proliferation and migration progression of VSMCs in atherosclerosis through the miR-181b/Notch1 axis.
Cardiac lipoma is extremely rare. Here we presented a unique
illustrative case of interatrial septal lipoma protruding into right
atrial causing symptoms in a 54-year-old male. Echocardiogram and
computed tomography showed a well-shaped, giant and fixed occupying
located in interatrial septum and right atrium. The only manifestation
was palpitation though the mass filled almost all atrium and compressed
superior vena cava. The patient received resection of the large-sized
lipoma sizing 87mm in diameter and weighing ~1000g.
Pathological exam demonstrated mature lipocytes and substantiated the
diagnosis of lipoma. The patient did well postoperatively and symptoms
were resolved.
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