Skip Navigation

Cardiovascular Research 2007 74(3):497-505; doi:10.1016/j.cardiores.2007.02.030
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
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
Google Scholar
Right arrow Articles by Tsai, Y.-C.
Right arrow Articles by Wang, D. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tsai, Y.-C.
Right arrow Articles by Wang, D. L.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2007, European Society of Cardiology

Laminar flow attenuates interferon-induced inflammatory responses in endothelial cells

Yu-Chih Tsaia, Hsyue-Jen Hsiehb, Fang Liaoa, Chih-Wen Nia, Yuen-Jen Chaoa, Chung-Yu Hsiehb and Danny Ling Wanga,*

aInstitute of Biomedical Sciences, Academia Sinica, Taipei 115, Taiwan
bDepartment of Chemical Engineering, National Taiwan University, Taipei 106, Taiwan

* Corresponding author. Cardiovascular Division, Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan. Tel.: +886 2 2652 3907; fax: +886 2 2782 9143. Email address: lingwang{at}ibms.sinica.edu.tw

Objective: Atherosclerosis is a chronic disease that involves inflammation, in which cytokines, including interferon-gamma (IFN{gamma}), participate. Endothelial cells (ECs) exposed to IFN{gamma} increase the expression of CXC chemokines. ECs subjected to laminar flow (LF) are atheroprotective, despite an unclear mechanism. This study was conducted to analyze whether ECs under LF were protected from IFN{gamma}-induced responses.

Methods: IFN{gamma}-treated human umbilical cord ECs were subjected to LF in a well-defined flow chamber system. IFN{gamma}-induced STAT1 activation and downstream target genes were examined.

Results: ECs exposed to IFN{gamma} triggered STAT1 activation via the phosphorylation of Tyr701 and Ser727 in STAT1. ECs exposed to LF alone did not activate STAT1. LF exposure of IFN{gamma}-treated ECs significantly attenuated IFN{gamma}-induced Tyr701 phosphorylation in a shear-force- and time-dependent manner, whereas Ser727 phosphorylation was unaffected. Consistently, LF inhibited IFN{gamma}-induced STAT1 binding to DNA. ECs treated with IFN{gamma} induced the expression of three T-cell-specific CXC chemokines (CXCL9, CXCL10 and CXCL11) as well as CIITA, a transcriptional regulator of major histocompatibility complex class II (MHCII). Consistently, LF exposure of IFN{gamma}-treated ECs reduced the expression of CXC chemokines and CIITA.

Conclusions: LF attenuates IFN{gamma}-induced responses via the suppression of STAT1 activation. Inhibition by LF of the interferon-induced ECs' response may explain some aspects of LF's atheroprotective effects on the endothelium.

KEYWORDS Endothelial cells; Laminar flow; Interferon-gamma; STAT1; CXC chemokines

Time for primary review 26 days


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




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.