Uremic Serum Induces Inflammation in Cultured Human Endothelial Cells and Triggers Vascular Repair Mechanisms
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ORIGINAL ARTICLE
Uremic Serum Induces Inflammation in Cultured Human Endothelial Cells and Triggers Vascular Repair Mechanisms Asmahan Eloueyk ,1,5 Bilal Osta,2 Rashad Alameldinne,3 and Dania Awad4
Inflammation and cardiovascular disease (CVD) are common in end-stage renal disease (ESRD) patients whose vascular endothelium is in direct contact with the uremic toxins found in the blood. These toxins are believed to affect vascular injury and repair process, which is impaired in ESRD patients. The exact mechanisms behind these interactions are not clear. So, we wanted to investigate what happens at the molecular level of endothelial cells when exposed to uremic serum from ESRD patients with diabetes and/or hypertension and its effect on the expression of molecules associated with vascular injury and repair. Cultured human endothelial cells (ECV304) were incubated in the presence of normal or uremic sera from ESRD patients with diabetes and/or hypertension. The expressions of monocyte chemoattractant protein 1 (MCP-1), vascular endothelial growth factor (VEGF), and stromal cell–derived factor 1 (SDF-1) were investigated in endothelial cells (ECV304) by real-time PCR and ELISA. The expression of MCP-1, VEGF, and SDF-1 was elevated in endothelial cells upon exposure to uremic sera from ESRD patients with diabetes and/or hypertension when compared with cells treated with healthy serum. MCP-1 expression in endothelial cells treated with uremic serum from ESRD patients with hypertension only was significantly increased compared with its expression in other cohorts. Exposure of endothelial cells to uremic serum causes endothelial injury and inflammation characterized by an increase in MCP-1 expression. This injury activates the initiation of vascular repair process in these cells by increasing the expression of VEGF and SDF-1. These molecules can be important biomarkers of chronic kidney disease–associated CVD.
Abstract—
KEY WORDS: uremia; endothelial cells; vascular injury; vascular repair; inflammation.
INTRODUCTION 1
Faculty of Science, Beirut Arab University, Debbieh, Lebanon Faculty of Science, Beirut Arab University, Tripoli, Lebanon 3 Orange Nassau Governmental Hospital, Tripoli, Lebanon 4 Faculty of Health Sciences 3, Lebanese University, Tripoli, Lebanon 5 To whom correspondence should be addressed at Faculty of Science, B e i r u t A r a b U n i v e r s i t y, D e b b i e h , L e b a n o n . E - m a i l : [email protected] 2
End-stage renal disease (ESRD) is classified under stage 5 of chronic kidney disease (CKD) where glomerular filtration rate (GFR), an estimate of kidney function calculated as follows: (186 × (creatinine/88.4) − 1.154 × (age) − 0.203 × (0.742 if female) × (1.210 if black), is lower than 15 mL/min/m2 of body area, or when patients are on
0360-3997/19/0000-0001/0 # 2019 Springer Science+Business Media, LLC, part of Springer Nature
Eloueyk, Osta, Alameldinne, and Awad dialysis regardless of their GFR [1]. Risk factors include older age (> 60 years), kidney disease history, obe
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