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Tumor necrosis factor induction of endothelial cell surface antigens is independent of protein kinase C activation or inactivation. Studies with phorbol myristate acetate and staurosporine.
J Immunol. 1991 May 01; 146(9):3056-62.JI

Abstract

We have investigated whether TNF-induced changes in human endothelial cell (EC) surface Ag expression are mediated by protein kinase C (PKC). This suggestion arose from the observations that PMA, a potent PKC activator, can mimic TNF by inducing expression of endothelial leukocyte adhesion molecule 1, intercellular adhesion molecule 1 (ICAM-1), and class I MHC molecules on human EC. However, in contrast to the actions of PMA, TNF neither causes membrane translocation of PKC nor induces the phosphorylation of the myristoylated alanine-rich C kinase substrate, two measures of PKC activation. Moreover, the PKC inhibitor staurosporine can block PMA-induced endothelial leukocyte adhesion molecule 1 expression at 4 h, but does not inhibit the actions of TNF. At 24 h, staurosporine itself induces intercellular adhesion molecule 1 and class I MHC, and acts additively with TNF. Twenty four hour treatment with PMA causes loss of PKC. We propose that at 24 h, staurosporine and PMA share a mechanism of action, namely diminution of PKC activity. However, 24 h treatment with TNF does not reduce the amount of PKC nor does it prevent activation of PKC by PMA. We conclude that TNF effects in EC are not mediated by PKC activation or inactivation.

Authors+Show Affiliations

Department of Pathology, Brigham and Women's Hospital, Boston, MA 02115.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

1707932

Citation

Ritchie, A J., et al. "Tumor Necrosis Factor Induction of Endothelial Cell Surface Antigens Is Independent of Protein Kinase C Activation or Inactivation. Studies With Phorbol Myristate Acetate and Staurosporine." Journal of Immunology (Baltimore, Md. : 1950), vol. 146, no. 9, 1991, pp. 3056-62.
Ritchie AJ, Johnson DR, Ewenstein BM, et al. Tumor necrosis factor induction of endothelial cell surface antigens is independent of protein kinase C activation or inactivation. Studies with phorbol myristate acetate and staurosporine. J Immunol. 1991;146(9):3056-62.
Ritchie, A. J., Johnson, D. R., Ewenstein, B. M., & Pober, J. S. (1991). Tumor necrosis factor induction of endothelial cell surface antigens is independent of protein kinase C activation or inactivation. Studies with phorbol myristate acetate and staurosporine. Journal of Immunology (Baltimore, Md. : 1950), 146(9), 3056-62.
Ritchie AJ, et al. Tumor Necrosis Factor Induction of Endothelial Cell Surface Antigens Is Independent of Protein Kinase C Activation or Inactivation. Studies With Phorbol Myristate Acetate and Staurosporine. J Immunol. 1991 May 1;146(9):3056-62. PubMed PMID: 1707932.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Tumor necrosis factor induction of endothelial cell surface antigens is independent of protein kinase C activation or inactivation. Studies with phorbol myristate acetate and staurosporine. AU - Ritchie,A J, AU - Johnson,D R, AU - Ewenstein,B M, AU - Pober,J S, PY - 1991/5/1/pubmed PY - 1991/5/1/medline PY - 1991/5/1/entrez SP - 3056 EP - 62 JF - Journal of immunology (Baltimore, Md. : 1950) JO - J Immunol VL - 146 IS - 9 N2 - We have investigated whether TNF-induced changes in human endothelial cell (EC) surface Ag expression are mediated by protein kinase C (PKC). This suggestion arose from the observations that PMA, a potent PKC activator, can mimic TNF by inducing expression of endothelial leukocyte adhesion molecule 1, intercellular adhesion molecule 1 (ICAM-1), and class I MHC molecules on human EC. However, in contrast to the actions of PMA, TNF neither causes membrane translocation of PKC nor induces the phosphorylation of the myristoylated alanine-rich C kinase substrate, two measures of PKC activation. Moreover, the PKC inhibitor staurosporine can block PMA-induced endothelial leukocyte adhesion molecule 1 expression at 4 h, but does not inhibit the actions of TNF. At 24 h, staurosporine itself induces intercellular adhesion molecule 1 and class I MHC, and acts additively with TNF. Twenty four hour treatment with PMA causes loss of PKC. We propose that at 24 h, staurosporine and PMA share a mechanism of action, namely diminution of PKC activity. However, 24 h treatment with TNF does not reduce the amount of PKC nor does it prevent activation of PKC by PMA. We conclude that TNF effects in EC are not mediated by PKC activation or inactivation. SN - 0022-1767 UR - https://www.unboundmedicine.com/medline/citation/1707932/Tumor_necrosis_factor_induction_of_endothelial_cell_surface_antigens_is_independent_of_protein_kinase_C_activation_or_inactivation__Studies_with_phorbol_myristate_acetate_and_staurosporine_ L2 - https://www.jimmunol.org/lookup/pmidlookup?view=long&pmid=1707932 DB - PRIME DP - Unbound Medicine ER -