The Induction of Intercellular Adhesion Molecule-1 on Human Umbilical Vein Endothelial Cells by a Heat-Stable Component of Porphyromonas gingivalis

2004 ◽  
Vol 48 (2) ◽  
pp. 108-112 ◽  
Author(s):  
Song Mao ◽  
Tsuyoshi Fujimura ◽  
Hiroshi Oda ◽  
Nobuaki Maeno ◽  
Seiken Matayoshi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Porphyromonas Gingivalis ◽  
Adhesion Molecule ◽  
Umbilical Vein ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Human Umbilical Vein ◽  
Stable Component ◽  
Heat Stable ◽  
Umbilical Vein Endothelial Cells

scholarly journals Human umbilical vein and dermal microvascular endothelial cells show heterogeneity in response to PKC activation

1997 ◽  
Vol 273 (4) ◽  
pp. C1233-C1240 ◽  
Author(s):  
Justin C. Mason ◽  
Helen Yarwood ◽  
Katharine Sugars ◽  
Dorian O. Haskard
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Morphological Changes ◽  
Umbilical Vein ◽  
Intercellular Adhesion Molecule ◽  
Microvascular Endothelial Cells ◽  
Intercellular Adhesion Molecule 1 ◽  
Human Umbilical Vein ◽  
Microvascular Endothelial ◽  
Pkc Activation

Changes in endothelial cell (EC) phenotype are central to the function of endothelium in inflammation. Although these events mainly occur in the microvasculature, previous studies have predominantly used large-vessel EC. Using enzyme-linked immunosorbent and flow cytometric assays, we compared the responses of human umbilical vein endothelial cells (HUVEC) and dermal microvascular endothelial cells (DMEC) to the activation of protein kinase C (PKC). Stimulation with phorbol 12,13-dibutyrate and more selective PKC agonists, including 12-deoxyphorbol 13-phenylacetate 20-acetate (dPPA), induced morphological changes and proliferation in both EC types. PKC activation induced a marked increase in Thy-1 expression on DMEC and only a moderate rise on HUVEC. Furthermore, heterogeneity in the induction of the adhesion molecules intercellular adhesion molecule 1, vascular cell adhesion molecule 1 (VCAM-1), and E-selectin between the two EC types following activation of PKC was demonstrated. In particular, E-selectin and VCAM-1 were significantly upregulated on HUVEC but not DMEC. The data indicate that the PKC pathway is unlikely to be important for E-selectin and VCAM-1 expression in the microvasculature but are consistent with a role for PKC in angiogenesis. This diversity in signaling in response to PKC activation may depend on differential utilization of PKC isozymes and may facilitate specialized endothelial responses.

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