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Blood, 15 July 2007, Vol. 110, No. 2, pp. 519-528.
Prepublished online as a Blood First Edition Paper on March 21, 2007; DOI 10.1182/blood-2006-08-040097.
 Previous Article | Table of Contents | Next Article 
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Mechanisms of induction of endothelial cell E-selectin expression by smooth muscle cells and its inhibition by shear stress
Jeng-Jiann Chiu1,2,
Li-Jing Chen1,
Chih-I Lee1,
Pei-Ling Lee1,
Ding-Yu Lee1,
Min-Chien Tsai1,
Chia-Wen Lin1,
Shunichi Usami3, and
Shu Chien3,5
1 Division of Medical Engineering Research, National Health Research Institutes, Miaoli, Taiwan, Republic of China;
2 Institute of Biomedical Engineering, National Yang-Ming University, Taipei, Taiwan, Republic of China;
3 Department of Bioengineering
4 Department of Medicine
5 Whitaker Institute of Biomedical Engineering, University of California San Diego, La Jolla
E-selectin is a major adhesion molecule expressed by endothelial cells (ECs), which are exposed to shear stress and neighboring smooth muscle cells (SMCs). We investigated the mechanisms underlying the modulation of EC E-selectin expression by SMCs and shear stress. SMC coculture induced rapid and sustained increases in expression of E-selectin and phosphorylation of interleukin-1 (IL-1) receptor-associated kinase glycoprotein-130, as well as the downstream mitogen-activated protein kinases (MAPKs) and Akt. By using specific inhibitors, dominant-negative mutants, and small interfering RNA, we demonstrated that activations of c-Jun-NH2-terminal kinase (JNK) and p38 of the MAPK pathways are critical for the coculture-induced E-selectin expression. Gel shifting and chromatin immunoprecipitation assays showed that SMC coculture increased the nuclear factor- B (NF-B)–promoter binding activity in ECs; inhibition of NF-B activation by p65-antisense, lactacystin, and N-acetyl-cysteine blocked the coculture-induced E-selectin promoter activity. Protein arrays and blocking assays using neutralizing antibodies demonstrated that IL-1ß and IL-6 produced by EC/SMC cocultures are major contributors to the coculture induction of EC signaling and E-selectin expression. Preshearing of ECs at 12 dynes/cm2 inhibited the coculture-induced EC signaling and E-selectin expression. Our findings have elucidated the molecular mechanisms underlying the SMC induction of EC E-selectin expression and the shear stress protection against this SMC induction.
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