A protein kinase C agonist, selective for the beta I isozyme, induces E-selectin and VCAM-1 expression on HUVEC but does not translocate PKC. Biochem Biophys Res Commun 1993 Jun 30;193(3):1283-90
Date
06/30/1993Pubmed ID
7686753DOI
10.1006/bbrc.1993.1764Scopus ID
2-s2.0-0027219052 (requires institutional sign-in at Scopus site) 34 CitationsAbstract
A protein kinase C (PKC) agonist selective for the beta I isozyme, 12-deoxyphorbol 13-phenylacetate 20-acetate (dPPA), induced NF-kappa B-like binding activity and surface expression of E-selectin and VCAM-1 in human umbilical vein endothelial cells (HUVEC), similar to the effects of tumor necrosis factor-alpha (TNF-alpha). Induction of E-selectin and VCAM-1 expression by dPPA was completely inhibited by the PKC inhibitors staurosporine and Ro31-7549. The PKC inhibitors also reduce TNF-alpha-induced VCAM-1 expression. However, neither dPPA nor TNF-alpha translocated PKC from the cytosolic to the plasma or nuclear membrane particulate fractions in HUVEC. These results indicate that activation of the beta I PKC isozyme is sufficient for expression of E-selectin and VCAM-1, and suggest that PKC may mediate the effects of TNF-alpha and dPPA without requiring the translocation normally associated with activation of PKC.
Author List
Deisher TA, Sato TT, Pohlman TH, Harlan JMAuthor
Thomas Sato MD Emeritus Professor in the Surgery department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AlkaloidsBase Sequence
Cell Adhesion Molecules
Cell Membrane
Cells, Cultured
Cytosol
E-Selectin
Endothelium, Vascular
Humans
Indoles
Isoenzymes
Kinetics
Maleimides
Membrane Glycoproteins
Molecular Sequence Data
NF-kappa B
Oligonucleotide Probes
Phorbol Esters
Promoter Regions, Genetic
Protein Kinase C
Staurosporine
Tetradecanoylphorbol Acetate
Tumor Necrosis Factor-alpha
Umbilical Veins
Vascular Cell Adhesion Molecule-1
