scholarly journals Tumour-derived interleukin 1α (IL-1α) up-regulates the release of soluble intercellular adhesion molecule-1 (sICAM-1) by endothelial cells

1997 ◽  
Vol 76 (10) ◽  
pp. 1255-1261 ◽  
Author(s):  
E Fonsatti ◽  
M Altomonte ◽  
S Coral ◽  
I Cattarossi ◽  
MR Nicotra ◽  
...  
2002 ◽  
Vol 76 (1) ◽  
pp. 427-431 ◽  
Author(s):  
Cheng-Hsien Chang ◽  
Yan Huang ◽  
Andrew C. Issekutz ◽  
May Griffith ◽  
Kuei-Hsiang Lin ◽  
...  

ABSTRACT A key event in virus-induced inflammation (leukocyte extravasation through the endothelium) is the local activation of endothelial cells, as indicated by the expression of adhesion molecules such as intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin. In order to identify triggers of inflammation in adenovirus infection, we inoculated respiratory and ocular epithelial cells with adenovirus type 37 (Ad37), a human pathogen associated with keratoconjunctivitis as well as urogenital and respiratory infections. Fluids from virus-infected epithelial cells activated ICAM-1 (and to a lesser extent, VCAM-1) expression on cultured human umbilical vein endothelial cells. Blocking studies with anticytokine antibodies implicated interleukin-1α (IL-1α) as the epithelial cell-derived factor which activated endothelial cell ICAM-1 expression. The results thus identify epithelial cell-derived IL-1α as a potentially important activator of endothelial cells in Ad37-induced inflammation.


2004 ◽  
Vol 50 (11) ◽  
pp. 2185-2187 ◽  
Author(s):  
Thomas C Register ◽  
Kathryn P Burdon ◽  
Leon Lenchik ◽  
Donald W Bowden ◽  
Gregory A Hawkins ◽  
...  

2018 ◽  
Vol 34 (2) ◽  
pp. 309-317 ◽  
Author(s):  
Vera S. Schellerer ◽  
Melanie C. Langheinrich ◽  
Veronika Zver ◽  
Robert Grützmann ◽  
Michael Stürzl ◽  
...  

2018 ◽  
Vol 19 (11) ◽  
pp. 3394 ◽  
Author(s):  
Mónica Muñoz-Vega ◽  
Felipe Massó ◽  
Araceli Páez ◽  
Gilberto Vargas-Alarcón ◽  
Ramón Coral-Vázquez ◽  
...  

Reverse cholesterol transport (RCT) is considered as the most important antiatherogenic role of high-density lipoproteins (HDL), but interventions based on RCT have failed to reduce the risk of coronary heart disease. In contrast to RCT, important evidence suggests that HDL deliver lipids to peripheral cells. Therefore, in this paper, we investigated whether HDL could improve endothelial function by delivering lipids to the cells. Internalization kinetics using cholesterol and apolipoprotein (apo) AI fluorescent double-labeled reconstituted HDL (rHDL), and human dermal microvascular endothelial cells-1 (HMEC-1) showed a fast cholesterol influx (10 min) and a slower HDL protein internalization as determined by confocal microscopy and flow cytometry. Sphingomyelin kinetics overlapped that of apo AI, indicating that only cholesterol became dissociated from rHDL during internalization. rHDL apo AI internalization was scavenger receptor class B type I (SR-BI)-dependent, whereas HDL cholesterol influx was independent of SR-BI and was not completely inhibited by the presence of low-density lipoproteins (LDL). HDL sphingomyelin was fundamental for intercellular adhesion molecule-1 (ICAM-1) downregulation in HMEC-1. However, vascular cell adhesion protein-1 (VCAM-1) was not inhibited by rHDL, suggesting that components such as apolipoproteins other than apo AI participate in HDL’s regulation of this adhesion molecule. rHDL also induced endothelial nitric oxide synthase eNOS S1177 phosphorylation in HMEC-1 but only when the particle contained sphingomyelin. In conclusion, the internalization of HDL implies the dissociation of lipoprotein components and a SR-BI-independent fast delivery of cholesterol to endothelial cells. HDL internalization had functional implications that were mainly dependent on sphingomyelin. These results suggest a new role of HDL as lipid vectors to the cells, which could be congruent with the antiatherogenic properties of these lipoproteins.


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