on February 17, 2005
Published online before print February 17, 2005, doi: 10.1161/01.ATV.0000159703.43374.19
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Submitted on September 28, 2004
Accepted on February 8, 2005
Shear Stress Inhibits Smooth Muscle Cell-Induced Inflammatory Gene Expression in Endothelial Cells. Role of NF-
B
Jeng-Jiann Chiu *;
From the Division of Medical Engineering Research (J.-J.C., L.-J.C., S.-F.C., P.-L.L., C.-I.L., M.-C.T., D.-Y.L.), National Health Research Institutes, Miaoli, Taiwan; the Institute of Biomedical Engineering (J.-J.L.), National Yang-Ming University, Taipei, Taiwan; and the Division of Biotechnology and Pharmaceutical Research (H.-P.H.), National Health Research Institutes, Miaoli, Taiwan, Republic of China; and the Departments of Bioengineering Medicine and Whitaker Institute of Biomedical (S.U., S.C.), Engineering, University of California San Diego, La Jolla, Calif.
* To whom correspondence should be addressed. E-mail: jjchiu{at}nhri.org.tw.
Objectives--Vascular endothelial cells (ECs) are influenced by shear stress and neighboring smooth muscle cells (SMCs). We investigated the inflammation-relevant gene expression in EC/SMC cocultures under static condition and in response to shear stress.
Materials and Methods--Under static condition, DNA microarrays and reverse-transcription polymerase chain reaction identified 23 inflammation-relevant genes in ECs whose expression was significantly affected by coculture with SMCs, with 18 upregulated and 5 downregulated. Application of shear stress (12 dynes/cm2) to the EC side of the coculture for 6 hours inhibited most of the proinflammatory gene expressions in ECs induced by coculture with SMCs. Inhibition of nuclear factor-
B (NF-B) activation by the p65-antisense, lactacystin, and N-acetyl-cysteine blocked the coculture-induced EC expression of proinflammatory genes, indicating that the NF-B binding sites in the promoters of these genes play a significant role in their expression as a result of coculture with SMCs. Chromatin immunoprecipitation assays demonstrated the in vivo regulation of NF-B recruitment to selected target promoters. Shear stress inhibited the SMC coculture-induced NF-B activation in ECs and monocytic THP-1 cell adhesion to ECs.
Conclusions--Our findings suggest that shear stress plays an inhibitory role in the proinflammatory gene expression in ECs located in close proximity to SMCs.
Key words: cDNA microarray • coculture • endothelial cells • shear stress • smooth muscle cells
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