Cell surface expression and serum levels of intercellular adhesion molecule-1 in renal cell carcinoma

1994 ◽  
Vol 22 (1) ◽  
pp. 9-15 ◽  
Author(s):  
R. Heicappell ◽  
J. Podlinski ◽  
H. Buszello ◽  
R. Ackermann
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Surface ◽  
Cell Carcinoma ◽  
Adhesion Molecule ◽  
Renal Cell ◽  
Serum Levels ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1

Molecular regulation of intercellular adhesion molecule 1 (ICAM-1) expression in renal cell carcinoma

1997 ◽  
Vol 25 (4) ◽  
pp. 231-238 ◽  
Author(s):  
K. Tanabe ◽  
S. C. Campbell ◽  
J. P. Alexander ◽  
F. Steinbach ◽  
M. G. Edinger ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Adhesion Molecule ◽  
Renal Cell ◽  
Intercellular Adhesion ◽  
Molecular Regulation ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1

scholarly journals Transcriptional Activation of mRNA of Intercellular Adhesion Molecule 1 and Induction of Its Cell Surface Expression in Normal Human Gingival Fibroblasts by Mycoplasma salivarium andMycoplasma fermentans

1999 ◽  
Vol 67 (6) ◽  
pp. 3061-3065 ◽  
Author(s):  
Li Dong ◽  
Ken-Ichiro Shibata ◽  
Yoshihiko Sawa ◽  
Akira Hasebe ◽  
Yuji Yamaoka ◽  
...  
Keyword(s):  
Cell Surface ◽  
Adhesion Molecule ◽  
Transcriptional Activation ◽  
Surface Expression ◽  
Intercellular Adhesion ◽  
Cell Surface Expression ◽  
Intercellular Adhesion Molecule ◽  
Gingival Tissue ◽  
Intercellular Adhesion Molecule 1 ◽  
Normal Human

ABSTRACT Lipoproteins in the cell membranes of both Mycoplasma salivarium and Mycoplasma fermentans were demonstrated to trigger the transcription of intercellular adhesion molecule-1 mRNA in normal fibroblasts isolated from human gingival tissue and to induce its cell surface expression by a mechanism distinct from that of Escherichia coli lipopolysaccharide. The lipid moiety of the lipoproteins was suggested to play a key role in the expression of the activity.

scholarly journals Shiga Toxin Selectively Upregulates Expression of Syndecan-4 and Adhesion Molecule ICAM-1 in Human Glomerular Microvascular Endothelium

Toxins ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 435
Author(s):  
Elena B. Volokhina ◽  
Wouter J. C. Feitz ◽  
Lonneke M. Elders ◽  
Thea J. A. M. van der Velden ◽  
Nicole C. A. J. van de Kar ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Shiga Toxin ◽  
Alternative Pathway ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Microvascular Endothelium ◽  
Protein Levels

Hemolytic uremic syndrome (HUS) is a severe renal disease that is often preceded by infection with Shiga toxin (Stx)-producing Escherichia coli (STEC). The exact mechanism of Stx-mediated inflammation on human glomerular microvascular endothelial cells (HGMVECs) during HUS is still not well understood. In this study, we investigated the effect of Stx1 on the gene expression of proteins involved in leucocyte-mediated and complement-mediated inflammation. Our results showed that Stx1 enhances the mRNA and protein expression of heparan sulfate proteoglycan (HSPG) syndecan-4 in HGMVECs pre-stimulated with tumor necrosis factor α (TNFα). CD44 was upregulated on mRNA but not on protein level; no effect on the mRNA expression of other tested HSPGs glypican-1 and betaglycan was observed. Furthermore, Stx1 upregulated the mRNA, cell surface expression, and supernatant levels of the intercellular adhesion molecule-1 (ICAM-1) in HGMVECs. Interestingly, no effect on the protein levels of alternative pathway (AP) components was observed, although C3 mRNA was upregulated. All observed effects were much stronger in HGMVECs than in human umbilical endothelial cells (HUVECs), a common model cell type used in endothelial studies. Our results provide new insights into the role of Stx1 in the pathogenesis of HUS. Possibilities to target the overexpression of syndecan-4 and ICAM-1 for STEC-HUS therapy should be investigated in future studies.

Action of cAMP on expression and release of adhesion molecules in human endothelial cells

1996 ◽  
Vol 270 (3) ◽  
pp. H807-H816 ◽  
Author(s):  
R. Morandini ◽  
G. Ghanem ◽  
A. Portier-Lemarie ◽  
B. Robaye ◽  
A. Renaud ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Umbilical Vein ◽  
Mrna Level ◽  
Phosphodiesterase Inhibitor ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Soluble E Selectin

The expression of E-selectin induced by tumor necrosis factor (TNF) on the surface of human umbilical vein endothelial cells (HUVEC) was partially inhibited by an increase in the level of adenosine 3',5'-cyclic monophosphate (cAMP), produced by forskolin or cholera toxin combined with the type IV phosphodiesterase inhibitor rolipram and the protein kinase A agonist phosphorothioate analogue of cAMP SpcAMPS. The same agents had no significant effect on the constitutive and TNF-stimulated expression of intercellular adhesion molecule 1 (ICAM-1), whereas the effect on vascular cell adhesion molecule 1 (VCAM-1) expression was variable depending on cell culture conditions. The stimulatory effects of phorbol 12-myristate 13-acetate and bacterial lipopolysaccharide (LPS) on E-selectin expression were also downregulated by the forskolin-rolipram combination and by SpcAMPS. Inhibition of the surface expression of E-selectin was associated with a decrease of the total amount of the protein in the cell lysate and a reduced mRNA level, with no significant effect on mRNA stability. In anesthetized rats, the terbutaline-rolipram combination reduced the rolling of leukocytes induced by LPS in the mesenteric microcirculation. In addition to their partial inhibitory effect on the TNF-induced surface expression of E-selectin on HUVEC, the forskolin-rolipram combination and SpcAMPS strongly inhibited the release of soluble E-selectin from these cells; the release of soluble ICAM-1 and VCAM-1 was unaffected by these agents. Isoproterenol reduced the release of soluble E-selectin, whereas it had no significant effect on the cell surface expression of the protein. This study underscores the potential anti-inflammatory effect of a rise in the endothelial cAMP level.

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