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Transverse Aortic Constriction in Mice
Published on: April 21, 2010
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Chronic NG-nitro-l-arginine methyl ester (L-NAME) administration in C57BL/6J mice induces a sustained decrease in
R J Ocsan1, Y N Lai, K V Prabhu
1Discipline of Pathology, Sydney Medical School, University of Sydney, Sydney, Australia. reperfusion@hotmail.com.
Summary
Chronic administration of NG-nitro-l-arginine methyl ester (L-NAME) causes cardiac hypertrophy. C-kit expression initially stable then decreases, suggesting cell differentiation rather than direct NOS inhibition.
Area of Science:
- Cardiovascular Biology
- Cellular Biology
- Molecular Medicine
Background:
- Chronic administration of NG-nitro-l-arginine methyl ester (L-NAME) is a validated rodent model for inducing cardiac hypertrophy.
- The role of c-kit expression in the development of cardiac hypertrophy remains incompletely understood.
Purpose of the Study:
- To investigate the expression patterns of c-kit in the context of L-NAME induced cardiac hypertrophy.
- To elucidate the potential involvement of c-kit positive cells in the pathogenesis of cardiac hypertrophy.
Main Methods:
- C57BL/6J mice were administered L-NAME in drinking water for up to 6 weeks.
- Cardiac hypertrophy was assessed by measuring ventricular wall thickness and cardiomyocyte cross-sectional area.
- Immunohistochemical staining was performed to evaluate c-kit expression in cardiac tissue.
Main Results:
- Six weeks of L-NAME administration resulted in significant cardiac hypertrophy.
- C-kit expression remained stable in the initial 1-2 days of L-NAME treatment but decreased significantly by day 5 and was sustained.
- C-kit positive cells were observed in both control and L-NAME treated mice, with predominant non-mast cell subtypes.
Conclusions:
- The decrease in c-kit expression after 5 days suggests it is not a direct consequence of nitric oxide synthase inhibition.
- The sustained presence of c-kit positive cells despite decreasing expression indicates potential differentiation into other cell types, possibly contributing to myocardial hyperplasia.

