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Cardiovascular Research 2004 64(1):154-164; doi:10.1016/j.cardiores.2004.06.014
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Inflammatory signaling pathway containing TRAF6 contributes to neointimal formation via diverse mechanisms

Takuya Miyaharaa,b,c, Hiroyuki Koyama*,a,b,c, Tetsuro Miyatab, Hiroshi Shigematsub, Jun-Ichiro Inoued, Tsuyoshi Takatoc and Hirokazu Nagawab

aDepartment of Vascular Regeneration, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo, Tokyo 113-8655, Japan
bDivision of Vascular Surgery, Department of Surgery, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo, Tokyo 113-8655, Japan
cDivision of Tissue Engineering, The University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo, Tokyo 113-8655, Japan
dDepartment of Oncology, The Institute of Medical Science, The University of Tokyo, 4-6-1, Shiroganedai, Minato, Tokyo 108-0071, Japan

* Corresponding author. 7-3-1 Hongo, Bunkyo, Tokyo 113-8655, Japan. Tel.: +81-3-5800-8653; fax: +81-3-3811-6822. E-mail address: hkoyama-tky{at}umin.ac.jp

Objective: The purpose of this study was to investigate the contribution of inflammatory signaling containing tumor necrosis factor receptor-associated factor 6 (TRAF6) to neointimal formation in a balloon injury model of rabbit carotid artery. Methods: Male Japanese white rabbits fed a normal diet were used. We transferred the dominant negative (DN) form of TRAF6 to a rabbit carotid artery that was subjected to balloon injury by in vivo electroporation method, and then evaluated its effect on intimal lesion formation after balloon injury. Results: An expression plasmid vector containing the TRAF6 DN sequence was successfully transferred to arterial wall cells, and its inhibitory effect on inflammatory signaling was confirmed by the marked suppression of nuclear factor-{kappa}B (NF{kappa}B) activity after injury. Morphometric analyses revealed significant inhibition of intimal lesion formation at 7 days after injury. Cell replication and accumulation of macrophages in the media were significantly decreased, and apoptosis was enhanced on day 2. Cell migration to the intima was suppressed on day 4. Extracellular signal-regulated kinase1/2 (ERK1/2) activity at 2 h after injury was also down-regulated. Interestingly, intimal cell replication was significantly blocked when TRAF6 DN was transfected at 7 days after injury. Conclusion: TRAF6 plays important roles in cell replication and migration, besides promotion of inflammatory cell infiltration and suppression of apoptosis.

KEYWORDS Intimal hyperplasia; Inflammatory signaling; Tumor necrosis factor receptor-associated factor 6; Nuclear factor-{kappa}B; Electroporation

Time for primary review 14 days


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