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Cardiovascular Research 2003 57(3):766-774; doi:10.1016/S0008-6363(02)00792-7
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Differential activation of matrix metalloproteinases in heart failure with and without ventricular dilatation

Nagahiro Nishikawaa, Kazuhiro Yamamotoa,*, Yasushi Sakataa, Toshiaki Manoa, Junichi Yoshidaa, Takeshi Miwab, Hiroshi Takedac, Masatsugu Horia and Tohru Masuyamaa

aDepartment of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita 565-0871, Japan
bGenome Information Research Center, Osaka University, Suita, Japan
cDepartment of Medical Information Science, Osaka University Graduate School of Medicine, Suita, Japan

kazuhiro{at}medone.med.osaka-u.ac.jp

* Corresponding author. Tel.: +81-6-6879-6612; fax: +81-6-6879-6613.

Objective: Remodeling of extracellular matrix (ECM) is considered to contribute to progression of left ventricular (LV) remodeling and matrix metalloproteinases (MMPs) play crucial roles in regulation of ECM. Activation of MMPs is observed in systolic heart failure (SHF) and is suggested to be responsible for LV dilatation in SHF. Diastolic heart failure (DHF) that is not associated with LV dilatation is also accompanied with collagen accumulation; however, differences in ECM regulatory system, especially activation of MMPs, between SHF and DHF remain to be clarified. This study was conducted to clarify whether MMPs are activated even in DHF, and if so, to characterize the difference in activation of MMPs between SHF and DHF for identification of a target for the prevention of LV remodeling in SHF. Methods: To exclude effects of differences in underling cardiovascular diseases and genetic background on the comparison between DHF and SHF, we used Dahl salt-sensitive rats fed on high salt diet starting at 7 weeks of age as DHF model and at 8 weeks as SHF model, both of which our laboratory recently developed. Results: LV fibrosis progressed in the DHF and SHF model rats. MMP-2 was activated to the same degree in both rats. Activation of MMP-9 was enhanced in the DHF model rats, but the activity was more enhanced in the SHF rats. Film in situ zymography showed that enhanced gelatinolytic activity appeared only in the mid layer of the LV wall in the DHF rats and throughout the wall in the SHF rats. The distribution of gelatinolytic activity was consistent with that of expression of MMP-9 as assessed in immunohistochemical study. Conclusions: MMP-9 rather than MMP-2 may be involved in LV dilatation in SHF and be a specific target for the prevention of LV remodeling.

KEYWORDS Extracellular matrix; Fibrosis; Heart failure; Hypertension; Remodeling


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