Background Hyperphosphatemia (HP) is associated with vascular calcification (VC) in chronic kidney disease (CKD). However, relationship between HP-induced-endothelial extracellular vesicles (HP-EC-EVs) and VC is unclear, and miR expression in HP-EC-EVs has not been determined. Methods We isolated HP-EC-EVs from endothelial cells with HP and observed that HP-EC-EVs were up-taken by vascular smooth muscle cells (VSMCs). HP-EC-EVs inducing calcium deposition was characterized by Alizarin Red S, colourimetric analysis and ALP activity. To investigate the mechanism of HP-EC-EVs-induced VSMC calcification, RNA-sequencing for HP-EC-EVs was performed. Results We first demonstrated that HP-EC-EVs induced VSMC calcification in vitro. RNA-seq analysis of HP-EC-EVs illustrated that one known miR (hsa-miR-3182) was statistically up-regulated and twelve miRs were significantly down-regulated, which was verified by qRT-PCR. We predicted 58,209 and 74,469 target genes for those down- and up-regulated miRs respectively through miRDB, miRWalk and miRanda databases. GO terms showed that down- and up-regulated targets were mostly enriched in calcium-dependent cell–cell adhesion via plama membrane cell-adhesion molecules (GO:0,016,338, BP) and cell adhesion (GO:0,007,155, BP), plasma membrane (GO:0,005,886, CC), and metal ion binding (GO:0,046,914, MF) and ATP binding (GO:0,005,524, MF) respectively. Top-20 pathways by KEGG analysis included calcium signaling pathway, cAMP signaling pathway, and ABC transporters, which were closely related to VC. Conclusion Our results indicated that those significantly altered miRs, which were packaged in HP-EC-EVs, may play an important role in VC by regulating related pathways. It may provide novel insight into the mechanism of CKD calcification.
BackgroundReduced left ventricular ejection function (LVEF) was associated with increased mortality in patients with peritoneal dialysis (PD) in Asia and the United States of America. The neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) were correlated with LVEF in PD. However, little information is available regarding the relationship between monocyte-to-lymphocyte ratio (MLR), left ventricular ejection fraction (LVEF), and the use of NLR, PLR, and MLR in predicting left ventricular systolic dysfunction (LVSD) in patients with PD.MethodsAll 181 patients with PD were enrolled between 2014 and 2021 from the Nephrology Department of the First Affiliated Hospital of the University of South China. Demographic features, clinical characteristics, laboratory values, and echocardiographic parameters were collected.ResultsThe mean age of patients with PD was 47.4 ± 12.6, and 90 (49.7%) of the patients were men. LVEF showed a negative correlation with PLR (r = −0.200, p = 0.007) and MLR (r = −0.146, p = 0.049). The levels of NLR, PLR, and MLR were elevated in patients with PD with LVSD compared with those without (all p < 0.05). PLR (OR 4.331, 95% CI: 1.223, 15.342) and albumin (OR 13.346, 95% CI: 3.928, 45.346) were significantly associated with LVSD patients with PD in the multivariate logistic analysis. For differentiating patients with PD with LVSD, optimal cutoffs of NLR, PLR, MLR, and albumin were 4.5 (sensitivity: 76.7%, specificity: 55.0%, and overall accuracy: 58%), 202.6 (sensitivity: 66.7%, specificity: 69.5%, and overall accuracy: 69%), 0.483 (sensitivity: 53.3%, specificity: 72.8%, and overall accuracy: 30%), and 34.6 (sensitivity: 72.2%), respectively.ConclusionsOur results revealed that PLR was better than NLR, MLR, and albumin in predicting LVSD in PD.
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