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TNFa‐Induced Expression of Endothelial Adhesion Molecules, ICAM‐1 and VCAM‐1, is Linked to Protein Kinase C Activation
Author(s) -
MATTILA P.,
MAJURI M.L.,
MATTILA P. S.,
RENKONEN R.
Publication year - 1992
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1992.tb03087.x
Subject(s) - protein kinase c , phorbol , vcam 1 , cell adhesion molecule , tumor necrosis factor alpha , microbiology and biotechnology , adhesion , icam 1 , chemistry , protein kinase a , intercellular adhesion molecule 1 , kinase , biology , immunology , organic chemistry
The role of protein kinase C (PKC) in TNFα‐induced activation of endothelial adhesion molecules ICAM‐1 and VCAM‐1 was analysed. Phorbol myristate acetate, which is known to activate PKC, was able lo mimic TNFα‐induced up‐regulation of ICAM‐1 and partly also VCAM‐1 expression. Similarly a PKC inhibitor, H7, but not another kinase inhibitor. HA1004, inhibited TNFα‐induced enhancement of ICAM‐1 expression at both the mRNA and the protein level. Moreover we were able to measure a transient PKC activation peak at 16 min after TNFα induction in endothelial cells analysed by phorbol‐dibutyrate binding. These results indicate that the TNFα‐induced effect on the regulation of endothelial adhesion molecule expression is at least partly mediated by PKC activation.