on October 28, 2004
Published online before print October 28, 2004, doi: 10.1161/01.ATV.0000148705.13411.65
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on November 13, 2003
Accepted on October 3, 2004
Granulocyte Macrophage-Colony Stimulating Factor Increases the Expression of Histamine and Histamine Receptors in Monocytes/Macrophages in Relation to Arteriosclerosis
Yoshitaka Murata ;
From the Kyurin Omtest Laboratory (Y.M.), Kyurin Corporation, Yahatanishi-ku, Kitakyushu, the Department of Pathology (A.T., H.M.), Toranomon Hospital and Okinaka Memorial Institute for Medical Research, Tokyo, and the Departments of Pathology and Cell Biology (A.T., K.-Y.W., Y.S.) and Pharmacology (M.T.), School of Medicine, University of Occupational and Environmental Health, Yahatanishi-ku, Kitakyushu, Japan; and Johnson and Johnson Pharmaceuticals Group (F.D.), Licensing and New Business Development, Beerse, Belgium.
* To whom correspondence should be addressed. E-mail: aki{at}toranomon.gr.jp.
Objective--To study the effect of granulocyte macrophage-colony-stimulating factor (GM-CSF) on histamine metabolism in arteriosclerosis, the expression of histidine decarboxylase (HDC; histamine-producing enzyme), histamine receptors 1 and 2 (HH1R and HH2R), and GM-CSF was investigated in human and mouse arteriosclerotic carotid arteries. Furthermore, the molecular mechanisms of GM-CSF-induced HDC and HH1R expression in monocytic U937 cells were investigated.
Methods and Results--Immunohistochemistry showed that atherosclerotic human coronary and mouse ligated carotid arteries contained HDC-expressing macrophages. Gene expression of HDC, HH1R, HH2R, and GM-CSF was also detected in the lesions. In U937 cells, GM-CSF enhanced histamine secretion and gene expression of HDC and HH1R. A promoter assay showed that GM-CSF enhanced gene transcription of HDC and HH1R but not HH2R.
Conclusion--The present results indicate that HDC and HHR are expressed in arteriosclerotic lesion, and that GM-CSF induces HDC and HH1R expression in monocytes. Locally produced histamine might participate in atherogenesis by affecting the expression of atherosclerosis-related genes in monocytes and smooth muscle cells.
Key words: monocyte/macrophage • histamine • histidine decarboxylase • histamine receptor • atherosclerosis
This article has been cited by other articles:
 |
|
 |
|
  A. Tanimoto, Y. Murata, K.-Y. Wang, M. Tsutsui, K. Kohno, and Y. Sasaguri Monocyte Chemoattractant Protein-1 Expression Is Enhanced by Granulocyte-Macrophage Colony-stimulating Factor via Jak2-Stat5 Signaling and Inhibited by Atorvastatin in Human Monocytic U937 Cells J. Biol. Chem., February 22, 2008; 283(8): 4643 - 4651. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. M. Hermann and C. M. Matter Tissue Plasminogen Activator Induced Reperfusion Injury After Stroke Revisited Circulation, July 24, 2007; 116(4): 363 - 365. [Full Text] [PDF]
|
|
|
|
 |
|
 A. Tanimoto, K.-Y. Wang, Y. Murata, S. Kimura, M. Nomaguchi, S. Nakata, M. Tsutsui, and Y. Sasaguri Histamine Upregulates the Expression of Inducible Nitric Oxide Synthase in Human Intimal Smooth Muscle Cells via Histamine H1 Receptor and NF-{kappa}B Signaling Pathway Arterioscler Thromb Vasc Biol, July 1, 2007; 27(7): 1556 - 1561. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Ditiatkovski, B.-H. Toh, and A. Bobik GM-CSF Deficiency Reduces Macrophage PPAR-{gamma} Expression and Aggravates Atherosclerosis in ApoE-Deficient Mice Arterioscler Thromb Vasc Biol, October 1, 2006; 26(10): 2337 - 2344. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Swan, S. A. Richards, N. P. Duroudier, I. Sayers, and I. P. Hall Alternative Promoter Use and Splice Variation in the Human Histamine H1 Receptor Gene Am. J. Respir. Cell Mol. Biol., July 1, 2006; 35(1): 118 - 126. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Sasaguri, K.-Y. Wang, A. Tanimoto, M. Tsutsui, H. Ueno, Y. Murata, Y. Kohno, S. Yamada, and H. Ohtsu Role of Histamine Produced by Bone Marrow-Derived Vascular Cells in Pathogenesis of Atherosclerosis Circ. Res., May 13, 2005; 96(9): 974 - 981. [Abstract] [Full Text] [PDF]
|
|