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Effects of histamine and interleukin‐4 synthesized in arterial intima on phagocytosis by monocytes/macrophages in relation to atherosclerosis
Author(s) -
Higuchi Satoshi,
Tanimoto Akihide,
Arima Nobuyuki,
Xu Hui,
Murata Yoshitaka,
Hamada Tetsuo,
Makishima Kazumi,
Sasaguri Yasuyuki
Publication year - 2001
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/s0014-5793(01)02823-x
Subject(s) - histidine decarboxylase , histamine , jurkat cells , scavenger receptor , phagocytosis , atheroma , monocyte , microbiology and biotechnology , chemistry , medicine , biology , endocrinology , immunology , histidine , biochemistry , immune system , t cell , enzyme , cholesterol , lipoprotein
We investigated the localization of histidine decarboxylase (HDC), which is the rate‐limiting enzyme that generates histamine from histidine, in human aorta/coronary artery. RT‐PCR and immunohistochemical staining revealed that the HDC gene was expressed in monocytes/macrophages and T cells in the arterial intima but not in smooth muscle cells in either the arterial intima or the media. A luciferase promoter assay with U937 and Jurkat cells demonstrated that interleukin‐4 (IL‐4) inhibited the expression of the HDC gene. In contrast, among a scavenger receptor family, IL‐4 as well as histamine up‐regulated U937 cells to express the LOX‐1 gene but not the SR‐A gene, which genes encode receptors that scavenge oxidized lipids. These findings suggest that histamine synthesized in the arterial wall participates in the initiation and progression of atherosclerosis and that IL‐4 can act as an important inhibitory and/or stimulatory factor in the function of monocytes/macrophages modulated by histamine in relation to the process of atherosclerosis.