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Cardiovascular Research Advance Access originally published online on July 31, 2008
Cardiovascular Research 2008 80(3):425-434; doi:10.1093/cvr/cvn202
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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

Granulocyte colony-stimulating factor exacerbates cardiac fibrosis after myocardial infarction in a rat model of permanent occlusion

Zhaokang Cheng1, Lailiang Ou1, Yi Liu1, Xiaolei Liu1, Fei Li2, Bin Sun1, Yongzhe Che3, Deling Kong1,*, Yaoting Yu1 and Gustav Steinhoff4

1 Key Laboratory of Bioactive Materials, Ministry of Education, College of Life Science, Nankai University, Tianjin 300071, China
2 Special Consulting Department, No. 254 Hospital of PLA, Tianjin, China
3 Medical College of Nankai University, Tianjin, China
4 Department of Cardiac Surgery, University of Rostock, Rostock, Germany

* Corresponding author. Tel: +86 22 23502111; fax: +86 22 23498775. E-mail address: kongdeling{at}nankai.edu.cn

Aims: Controversy exists regarding the effects of granulocyte colony-stimulating factor (G-CSF) on post-infarction remodelling, which is regulated by matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). The aim of this study was to investigate the impact of G-CSF administration on cardiac MMP/TIMP ratios and long-term remodelling in a rat model of acute myocardial infarction (MI).

Methods and results: Sprague–Dawley rats underwent coronary ligation to produce MI. Rats surviving the MI for 3 h were randomized to receive G-CSF (50 µg/kg/day for 5 consecutive days, n = 16) or saline (n = 10). Sham-operated animals received no treatment (n = 10). G-CSF injection significantly increased circulating white blood cells, neutrophils, and monocytes. Western blotting revealed that the ratios of MMP-2/TIMP-1 and MMP-9/TIMP-1 were significantly decreased in the infarcted myocardium. At 3 months, echocardiographic and haemodynamic examinations showed that the G-CSF treatment induced left ventricular (LV) enlargement and dysfunction. Histological analysis revealed that the extent of myocardial fibrosis and infarct size were larger in the G-CSF group than in the Saline group. Furthermore, G-CSF treated animals showed a significantly lower post-MI survival during the study period.

Conclusion: Decrease of cardiac MMP/TIMP ratios by G-CSF after infarction may be important as a mechanism in promotion of myocardial fibrosis, which further facilitates infarct expansion and LV dysfunction.

KEYWORDS G-CSF; Myocardial infarction; Fibrosis; Infarct expansion; Remodelling

Time for primary review: 34 days


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