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Wen W.,Xian Jiaotong University | Wan Z.,Xian Jiaotong University | Ren K.,Xian Jiaotong University | Zhou D.,Xian Jiaotong University | And 7 more authors.
Experimental and Molecular Pathology | Year: 2016

High salt intake contributes to the development of autoimmune/inflammatory diseases, while potassium supplementation antagonizes the effects. Interleukin (IL)-17A are tightly related with autoimmune/inflammatory diseases. Thus, we explored the effects and underlying molecular mechanism of high salt and potassium supplementation on IL-17A production in T lymphocytes. Forty-nine healthy participants received a low-salt, high-salt, followed by a high-salt diet plus potassium supplement for 7 days, respectively. Human T lymphocyte Jurkat cells were treated with different concentrations of NaCl and KCl. In the participants, IL-17A levels in plasma and in peripheral blood mononuclear cells (PBMC) were significantly increased after a high-salt diet, which was dramatically reversed when potassium was supplemented. In Jurkat cells, the addition of 40 mM NaCl markedly enhanced IL-17A production and the expression of phosphorylated p38/mitogen-activated protein kinase (MAPK) and its downstream target, serum/glucocorticoid-regulated kinase (SGK)1, whereas combined treatment with additional 2 mM KCl significantly decreased them. Respective inhibition of p38/MAPK and SGK1 suppressed IL-17A expression induced by NaCl, and KCl inhibited IL-17A production induced by specific activator of p38/MAPK. We conclude potassium supplementation has a blocking effect on IL-17A production in T lymphocytes induced by salt loading. This protective effect is mediated through the direct suppression of p38/MAPK-SGK1 pathway. © 2016 Elsevier Inc. Source


Bai L.,Shaanxi Key Laboratory of Molecular Cardiology | Liu P.,Shaanxi Key Laboratory of Molecular Cardiology | Ma A.-Q.,Shaanxi Key Laboratory of Molecular Cardiology | Du Y.,Shaanxi Key Laboratory of Molecular Cardiology | And 3 more authors.
Journal of Xi'an Jiaotong University (Medical Sciences) | Year: 2014

Objective: To investigate the mechanisms of antiphospholipid antibody (APA) inducing atherosclerosis (AS) by observing the effects of APA on the formation of macrophage-derived foam cell line from human U937 cell line induced by oxidized low density lipoprotein (ox-LDL) and the secretion of vascular endothelial growth factor (VEGF).Methods: U937 cells were incubated with ox-LDL or ox-LDL and APA together to induce the transformation of U937 into foam cells. The contents of cholesterol and cholesterol ester, apoptosis, and secretion of VEGF were observed by cell culture method, enzyme-fluorometric method, transmission electron microscopy, DNA gel electrophoresis and enzyme-linked immunosorbent assay.Results: After incubation with ox-LDL, the contents of cholesterol and cholesterol ester in U937 cells increased from (215±10)mg/g cell protein and (87±10)mg/g cell protein to (243±7)mg/g cell protein and (226±12)g/g cell protein, respectively. When the U937 cells were incubated with APA and ox-LDL together, the contents of cholesterol and cholesterol ester increased to a higher level of (276±10)mg/g cell protein and (384±13)mg/g cell protein; foam cells and apoptotic cells appeared. The secretion of VEGF also increased from (2 331±178)pg/mL to (2 716±145)pg/mL.Conclusion: APA can promote the intake of ox-LDL by U937 cells, induce apoptosis, accelerate the transformation of foam cells, and elevate the secretion of VEGF. Source

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