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The role of protein kinase C in the induction of VCAM‐1 expression on human umbilical vein endothelial cells
Author(s) -
Deisher Theresa A.,
Haddix Terri L.,
Montgomery Kevin F.,
Pohlman Timothy H.,
Kaushansky Kenneth,
Harlan John M.
Publication year - 1993
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(93)80354-w
Subject(s) - umbilical vein , vcam 1 , protein kinase a , microbiology and biotechnology , chemistry , kinase , biology , biochemistry , icam 1 , in vitro , cell adhesion molecule
The role of protein kinase C (PKC) in interleukin‐1β‐ (II‐ 1β)‐, tumor necrosis factor‐α‐ (TNF‐α)‐, and lipopolysaccharide‐(LPS)‐induced vascular cell adhesion molecule‐1 (VCAM‐1) expression on human umbilical vein endothelial cells (HUVEC) was studied. PKC inhibition or downregulation diminished VCAM‐1 mRNA accumulation and protein expression. Interleukin‐1β, TNF‐α, and LPS induce nuclear factor (NF)‐ k B‐like binding activity, which precedes VCAM‐1 transcription. PKC inhibition did not prevent NF‐ x B‐like binding activity, indicating that this is PKC‐independent, and NF‐ k B‐like binding activity is insufficient for transcription of VCAM‐1.