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Am J Physiol Heart Circ Physiol (February 6, 2003). doi:10.1152/ajpheart.00873.2002
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Submitted on October 4, 2002
Accepted on February 3, 2003

Unloading-induced remodeling in the normal and hypertrophic left ventricle

Brian S. McGowan1*, Christopher B. Scott2, Anbin Mu1, Richard J. McCormick3, D. Paul Thomas2, and Kenneth B. Margulies1

1 Department of Cardiovascular Research Group, Temple University School of Medicine, Philadelphia, PA, USA
2 Division of Kinesiology and Health, University of Wyoming, Laramie, WY, USA
3 Department of Animal Science, University of Wyoming, Laramie, WY, USA

* To whom correspondence should be addressed. E-mail: brianmcgowan{at}usa.net.

Background: To date, no study has assessed the degree of similarity between left ventricular (LV) reverse remodeling and atrophic remodeling. Methods: Stable LV hypertrophy was induced by creation of an arterio-venous fistula (AVF) in Lewis rats (32 days). LV unloading was induced by heterotopic transplantation of normal (NL-HT) and/or hypertrophic (AVF-HT) hearts (7 days). We compared indices of remodeling in AVF, NL-HT, AVF-HT groups, with those of normal controls (NL). Results: LV unloading induced decreases in cardiomyocyte size in NL-HT and AVF-HT hearts. NL-HT and AVF-HT LV were both characterized by relative increases in collagen concentration that was largely a reflection of decreases in myocyte volume. NL-HT and AVF-HT LV were associated with similar increases in matrix metalloproteinase (MMP-2 and MMP-9) zymographic activity, without change in the abundance of the tissue inhibitors of the matrix metalloproteinases (TIMPs). In contrast, AVF-HT, but not NL-HT, was associated with a dramatic increase in collagen crosslinking. Conclusions: Our findings suggest an overall similarity in the response of the normal and hypertrophic LV to surgical unloading. However, the dramatic increase in collagen crosslinking following just one week of unloading suggests a potential difference in the dynamics of collagen metabolism between the two models. Further studies will be required to determine the precise molecular mechanisms responsible for these differences in ECM regulation. However, with respect to these and related issues, heterotopic transplantation of hypertrophied hearts will be a useful small animal model for defining mechanisms of myocyte-matrix interations during decreased loading conditions.




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