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Cardiovascular Research Advance Access first published online on June 16, 2008
This version [Corrected Proof] published online on July 7, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn163
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

High-mobility group box 1 restores cardiac function after myocardial infarction in transgenic mice

Tatsuro Kitahara1, Yasuchika Takeishi2,*, Mutsuo Harada1, Takeshi Niizeki1, Satoshi Suzuki1, Toshiki Sasaki1, Mitsunori Ishino1, Olga Bilim1, Osamu Nakajima3 and Isao Kubota1

1 Department of Cardiology, Pulmonology and Nephrology, Yamagata University School of Medicine, Yamagata, Japan
2 First Department of Internal Medicine, Fukushima Medical University, 1 Hikarigaoka, Fukushima 960-1295, Japan
3 Research Laboratory for Molecular Genetics, Yamagata University School of Medicine, Yamagata, Japan

* Corresponding author. Tel: +81 24 547 1188; fax: +81 24 548 1821. E-mail address: takeishi{at}fmu.ac.jp

Aims: High-mobility group box 1 (HMGB1) is a nuclear DNA-binding protein and is released from necrotic cells, inducing inflammatory responses and promoting tissue repair and angiogenesis. To test the hypothesis that HMGB1 enhances angiogenesis and restores cardiac function after myocardial infarction (MI), we generated transgenic mice with cardiac-specific overexpression of HMGB1 (HMGB1-Tg) using {alpha}-myosin heavy chain promoter.

Methods and results: The left anterior descending coronary artery was ligated in HMGB1-Tg and wild-type littermate (Wt) mice. After coronary artery ligation, HMGB1 was released into circulation from the necrotic cardiomyocytes of HMGB1-overexpressing hearts. The size of MI was smaller in HMGB1-Tg than in Wt mice. Echocardiography and cardiac catheterization demonstrated that cardiac remodelling and dysfunction after MI were prevented in HMGB1-Tg mice compared with Wt mice. Furthermore, the survival rate after MI of HMGB1-Tg mice was higher than that of Wt mice. Immunohistochemical staining revealed that capillary and arteriole formation after MI was enhanced in HMGB1-Tg mice.

Conclusion: We report the first in vivo evidence that HMGB1 enhances angiogenesis, restores cardiac function, and improves survival after MI. These results may provide a novel therapeutic approach for left ventricular dysfunction after MI.

KEYWORDS HMGB1; Cardiac remodelling; Myocardial infarction; Angiogenesis

Time for primary review: 20 days


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