5-Lipoxygenase facilitates healing after myocardial infarction
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- 作者：Nadja Bl?mer (1)
Christina Pachel (1)
Ulrich Hofmann (1) (2)
Peter Nordbeck (1) (2)
Wolfgang Bauer (1) (2)
Denise Mathes (1)
Anna Frey (1) (2)
Barbara Bayer (1) (2)
Benjamin Vogel (1) (2)
Georg Ertl (1) (2)
Johann Bauersachs (3)
Stefan Frantz (1) (2) - 关键词：Myocardial infarction ; Extracellular matrix remodeling ; Inflammation ; Lipoxygenase
- 刊名：Basic Research in Cardiology
- 出版年：2013
- 出版时间：July 2013
- 年：2013
- 卷：108
- 期：4
- 全文大小：500 KB
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Christina Pachel (1)
Ulrich Hofmann (1) (2)
Peter Nordbeck (1) (2)
Wolfgang Bauer (1) (2)
Denise Mathes (1)
Anna Frey (1) (2)
Barbara Bayer (1) (2)
Benjamin Vogel (1) (2)
Georg Ertl (1) (2)
Johann Bauersachs (3)
Stefan Frantz (1) (2)
1. Department of Internal Medicine I, University Hospital Würzburg, Würzburg, Germany
2. Comprehensive Heart Failure Center, University of Würzburg, Oberdürrbacher Stra?e 6, 97080, Würzburg, Germany
3. Department of Cardiology and Angiology, Medizinische Hochschule Hannover, Hannover, Germany - ISSN：1435-1803
文摘
Early healing after myocardial infarction (MI) is characterized by a strong inflammatory reaction. Most leukotrienes are pro-inflammatory and are therefore potential mediators of healing and remodeling after myocardial ischemia. The enzyme 5-lipoxygenase (5-LOX) has a key role in the transformation of arachidonic acid in leukotrienes. Thus, we tested the effect of 5-LOX on healing after MI. After chronic coronary artery ligation, early mortality was significantly increased in 5-LOX??/sup> when compared to matching wildtype (WT) mice due to left ventricular rupture. This effect could be reproduced in mice treated with the 5-LOX inhibitor Zileuton. A perfusion mismatch due to the vasoactive potential of leukotrienes is not responsible for left ventricular rupture since local blood flow assessed by magnetic resonance perfusion measurements was not different. However, after MI, there was an accentuation of the inflammatory reaction with an increase of pro-inflammatory macrophages. Yet, mortality was not changed in chimeric mice (WT vs. 5-LOX??/sup> bone marrow in 5-LOX??/sup> animals), indicating that an altered function of 5-LOX??/sup> inflammatory cells is not responsible for the phenotype. Collagen production and accumulation of fibroblasts were significantly reduced in 5-LOX??/sup> mice in vivo after MI. This might be due to an impaired migration of 5-LOX??/sup> fibroblasts, as shown in vitro to serum. In conclusion, a lack or inhibition of 5-LOX increases mortality after MI because of healing defects. This is not mediated by a change in local blood flow, but through an altered inflammation and/or fibroblast function.