Skip Navigation

Cardiovascular Research 1998 37(3):820-825; doi:10.1016/S0008-6363(97)00265-4
© 1998 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Ikeda, U.
Right arrow Articles by Shimada, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ikeda, U.
Right arrow Articles by Shimada, K.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 1998, European Society of Cardiology

Monocyte–vascular smooth muscle cell interaction enhances nitric oxide production

Uichi Ikedaa,*, Yoshikazu Maedaa, Hiroshi Funayamaa, Yukihiro Hojoa, Michiyo Ikedab, Seiji Minotab, Shogo Kanob and Kazuyuki Shimadaa

aDepartment of Cardiology, Jichi Medical School, Tochigi, Japan
bDepartment of Clinical Immunology, Jichi Medical School, Tochigi, Japan

* Corresponding author. Department of Cardiology, Jichi Medical School, Minamikawachi-machi, Tochigi 329-04, Japan. Tel. (+81-285) 44-2111, ext. 3556; Fax (+81-285) 44-5317; E-mail: uikeda@jichi.ac.jp

Objective: The adhesive interaction of monocytes and vascular smooth muscle cells (VSMCs) has been suggested to be a regulatory signal in the cellular activation that is involved in the pathogenesis of atherosclerosis. We investigated the effects of monocyte–VSMC interaction on inducible nitric oxide (NO) synthase expression. Methods: NO production by the cultured cells was determined by measuring the nitrite content of the culture media using the Griess reagent. The expression of inducible NO synthase protein was assayed by Western blotting. Results: Interleukin-1β (IL-1β) induced nitrite production by VSMCs in a time-dependent manner. The addition of the mouse monocyte cell line J774 to IL-1β-stimulated VSMCs further increased nitrite production in a monocyte number-dependent manner. Enhanced nitrite production by coculture was accompanied by increased inducible NO synthase protein accumulation. Addition of tumor necrosis factor-{alpha} (TNF-{alpha}) also enhanced IL-1β-induced nitrite production by VSMCs, but TNF-{alpha} showed no effect in the presence of monocytes. Coculture of monocytes and VSMCs in the presence of IL-1β secreted substantial amounts of TNF-{alpha}. The production of nitrite by coculture was markedly inhibited by an anti-TNF-{alpha} antibody. Conclusions: The present study revealed that direct cell-to-cell interaction between monocytes and VSMCs enhances NO production, suggesting an important role for their interaction in the pathogenesis of atherosclerosis.

KEYWORDS Monocyte; Vascular smooth muscle; Nitrite; Atherosclerosis


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Innate ImmunityHome page
H. Loppnow, K. Werdan, and M. Buerke
Invited review: Vascular cells contribute to atherosclerosis by cytokine- and innate-immunity-related inflammatory mechanisms
Innate Immunity, April 1, 2008; 14(2): 63 - 87.
[Abstract] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.