Laminar flow attenuates interferon-induced inflammatory responses in endothelial cells

doi:10.1016/j.cardiores.2007.02.030

Cardiovascular Research 2007 74(3):497-505; doi:10.1016/j.cardiores.2007.02.030

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Laminar flow attenuates interferon-induced inflammatory responses in endothelial cells

Yu-Chih Tsai^a, Hsyue-Jen Hsieh^b, Fang Liao^a, Chih-Wen Ni^a, Yuen-Jen Chao^a, Chung-Yu Hsieh^b and Danny Ling Wang^a^,*

^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 involvesinflammation, in which cytokines, including interferon-gamma(IFN ${gamma}$ ), participate. Endothelial cells (ECs) exposed to IFN ${gamma}$ increasethe expression of CXC chemokines. ECs subjected to laminar flow(LF) are atheroprotective, despite an unclear mechanism. Thisstudy was conducted to analyze whether ECs under LF were protectedfrom IFN ${gamma}$ -induced responses.

Methods: IFN ${gamma}$ -treated human umbilical cord ECs were subjectedto LF in a well-defined flow chamber system. IFN ${gamma}$ -induced STAT1activation and downstream target genes were examined.

Results: ECs exposed to IFN ${gamma}$ triggered STAT1 activation via thephosphorylation of Tyr701 and Ser727 in STAT1. ECs exposed toLF alone did not activate STAT1. LF exposure of IFN ${gamma}$ -treatedECs significantly attenuated IFN ${gamma}$ -induced Tyr701 phosphorylationin a shear-force- and time-dependent manner, whereas Ser727phosphorylation was unaffected. Consistently, LF inhibited IFN ${gamma}$ -inducedSTAT1 binding to DNA. ECs treated with IFN ${gamma}$ induced the expressionof three T-cell-specific CXC chemokines (CXCL9, CXCL10 and CXCL11)as well as CIITA, a transcriptional regulator of major histocompatibilitycomplex class II (MHCII). Consistently, LF exposure of IFN ${gamma}$ -treatedECs reduced the expression of CXC chemokines and CIITA.

Conclusions: LF attenuates IFN ${gamma}$ -induced responses via the suppressionof STAT1 activation. Inhibition by LF of the interferon-inducedECs' response may explain some aspects of LF's atheroprotectiveeffects on the endothelium.

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

Time for primary review 26 days

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