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Induction of Endothelial Platelet‐Derived Growth Factor‐B‐Chain and Intercellular Adhesion Molecule‐1 by Lysophosphatidylcholine a
Author(s) -
KITA T.,
KUME N.,
OCHI H.,
NISHI E.,
SAKAI A.,
ISHII K.,
NAGANO Y.,
YOKODE M.
Publication year - 1997
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1997.tb51990.x
Subject(s) - downregulation and upregulation , lysophosphatidylcholine , platelet derived growth factor receptor , microbiology and biotechnology , protein kinase c , signal transduction , growth factor , platelet derived growth factor , intracellular , biology , intercellular adhesion molecule 1 , chemistry , biochemistry , phospholipid , receptor , gene , membrane , phosphatidylcholine
Lysophosphatidylcholine (lyso-PC) is a major phospholipid component of atherogenic lipoproteins. Lyso-PC has been shown to differentially upregulate the adhesion molecules, such as VCAM-1 and ICAM-1, as well as smooth muscle growth factors, such as PDGF-A, B chains and HB-EGF gene expression in various cultured endothelial cells. In this paper, we demonstrate increased expression of cell- and matrix-associated forms of PDGF-B protein elicited by lyso-PC and further characterized potential signal transduction mechanisms responsible for lyso-PC-induced human umbilical vein endothelial cell. Cycloheximide inhibited PDGF-B but not ICAM-1 mRNA induction by lyso-PC, suggesting the dependence on de novo protein synthesis for PDGF-B, but not ICAM-1. A protein kinase C (PKC) inhibitor did not block lyso-PC-induced increases in PDGF-B or ICAM-1 mRNA. The elevated level of cAMP blocked both PDGF-B and ICAM-1 upregulation by lyso-PC. However cAMP-elevating agents did not suppress ICAM-1 upregulation by PMA. Taken together, PDGF-B and ICAM-1 gene induction by lyso-PC may involve different signaling mechanisms; however, both appear to be independent of PMA-regulatable PKC activation but are suppressed by increased levels of intracellular cAMP.