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Circulation Research. 2001
Published online before print September 27, 2001, doi: 10.1161/hh2201.099373
A more recent version of this article appeared on November 9, 2001
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Submitted on March 8, 2001
Revised on September 18, 2001
Accepted on September 18, 2001

cis Element Decoy Against Nuclear Factor-{kappa}B Attenuates Development of Experimental Autoimmune Myocarditis in Rats

Osamu Yokoseki , Jun-ichi Suzuk , Hiroshi Kitabayashi , Noboru Watanabe , Yuko Wada , Motokuni Aoki , Ryuichi Morishita , Yasufumi Kaneda , Toshio Ogihara , Hideki Futamatsu , Yasushi Kobayashi , and Mitsuaki Isobe *

From the Departments of Internal Medicine I (O.Y., J.S., H.K., N.W., M.I.) and Surgery II (Y.W.), Shinshu University School of Medicine, Nagano, Japan; the Division of Gene Therapy Science (M.A., R.M., Y.K.) and the Department of Geriatric Medicine (T.O.), Osaka University Faculty of Medicine, Osaka, Japan; and the Department of Cardiovascular Medicine (H.F., Y.K., M.I.), Tokyo Medical and Dental University School of Medicine, Tokyo, Japan.

* To whom correspondence should be addressed. E-mail: isobemi.cvm{at}tmd.ac.jp.

Nuclear factor-{kappa}B (NF{kappa}B) plays a significant role in the coordinated transactivation of cytokine, inducible NO synthase (iNOS), and adhesion molecule genes. Although inflammation is an essential pathological feature of myocarditis, the role of NF{kappa}B in this process remains obscure. We examined the role of NF{kappa}B in the progression of rat experimental autoimmune myocarditis (EAM) and tested the hypothesis that NF{kappa}B blockade with a decoy against the cis element of NF{kappa}B can prevent the progression of EAM. Lewis rats were immunized with purified porcine cardiac myosin to establish EAM on day 0. NF{kappa}B decoy was infused into the rat coronary artery on day 0 (group NF0), 7 (group NF7), or 14 (group NF14) and harvested on day 21. Scrambled decoy was infused on day 0 (group SD0), 7 (group SD7), or 14 (group SD14) and served for control groups. The ratios of myocarditis-affected areas to the ventricular cross-sectional area of all treatment groups were significantly lower than those of the control groups (group NF0, 33±18% versus SD0, 53±14%; group NF7, 19±15% versus SD7, 50±16%; and group NF14, 34±10% versus SD14, 52±14%). Immunohistochemical and immunoblot analyses showed expression of ICAM-1, iNOS, IL-2, and TNF{alpha} in myocardium of scrambled decoy groups, and this expression was effectively suppressed by NF{kappa}B decoy treatment. Thus, we found that NF{kappa}B is a key regulator in the progression of EAM and that in vivo transfection of NF{kappa}B decoy reduces the severity of EAM.


Key words: myocarditis • gene therapy • nuclear factor-{kappa}B




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