scholarly journals Mixed Lineage Kinase Domain-Like Protein Promotes Human Monocyte Cell Adhesion to Human Umbilical Vein Endothelial Cells Via Upregulation of Intercellular Adhesion Molecule-1 Expression

2020 ◽  
Vol 26 ◽  
Author(s):  
Fen Cai ◽  
Jia-Li Wang ◽  
Yi-Lin Wu ◽  
Yan-Wei Hu ◽  
Qian Wang
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Umbilical Vein ◽  
Human Monocyte ◽  
Kinase Domain ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Mixed Lineage Kinase ◽  
Monocyte Cell ◽  
Umbilical Vein Endothelial Cells

scholarly journals Hyperketonemia increases monocyte adhesion to endothelial cells and is mediated by LFA-1 expression in monocytes and ICAM-1 expression in endothelial cells

2011 ◽  
Vol 301 (2) ◽  
pp. E298-E306 ◽  
Author(s):  
Justin L. Rains ◽  
Sushil K. Jain
Keyword(s):  
Endothelial Cells ◽  
Vascular Disease ◽  
Adhesion Molecule ◽  
Umbilical Vein ◽  
Intercellular Adhesion Molecule ◽  
Lymphocyte Function ◽  
Monocyte Adhesion ◽  
Intercellular Adhesion Molecule 1 ◽  
Monocyte Cell ◽  
Umbilical Vein Endothelial Cells

Frequent episodes of hyperketonemia are associated with a higher incidence of vascular disease. The objective of this study was to examine the hypothesis that hyperketonemia increases monocyte-endothelial cell (EC) adhesion and the development of vascular disease in diabetes. Human U937 and THP-1 monocyte cell lines and human umbilical vein endothelial cells (HUVECs) were cultured with acetoacetate (AA) (0–10 mM) or β-hydroxybutyrate (BHB) (0–10 mM) for 24 h prior to evaluating adhesion and adhesion molecule expression. The results demonstrate a significant ( P < 0.01) increase in both U937 and THP-1 adhesion to HUVEC monolayers treated with 4 mM AA compared with control. Equal concentrations of BHB resulted in similar increases in monocyte-EC adhesion. Similarly, treatments of AA or BHB to isolated monocytes from human blood also show increases in adhesion to endothelial cells. intercellular adhesion molecule-1 (ICAM-1) was significantly increased on the surface of HUVECs and an increase in total protein expression with AA treatment compared with control. The expression level of lymphocyte function-associated antigen-1 (LFA-1) was increased in monocytes treated with AA, and LFA-1 affinity was altered from low to high affinity following treatment with both AA and BHB. Monocyte adhesion could be blocked when cells were preincubated with an antibody to ICAM-1 or LFA-1. Results also show a significant increase in IL-8 and MCP-1 secretion in monocytes and HUVECs treated with 0–10 mM AA. These results suggest that hyperketonemia can induce monocyte adhesion to endothelial cells and that it is mediated via increased ICAM-1 expression in endothelial cells and increased expression and affinity of LFA-1 in monocytes.

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