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- Title
A Cell-permeable NFAT Inhibitor Peptide Prevents Pressure-Overload Cardiac Hypertrophy.
- Authors
Kuriyama, Mitsuhito; Matsushita, Masayuki; Tateishi, Atsushi; Moriwaki, Akiyoshi; Tomizawa, Kazuhito; Ishino, Kozo; Sano, Shunji; Matsui, Hideki
- Abstract
The activation of the calcineurin–nuclear factor of activated T cells cascade during the development of pressure-overload cardiac hypertrophy has been previously reported in a number of studies. In addition, numerous pharmacological studies involving calcineurin inhibitors such as FK506 and cyclosporine A have now demonstrated that these agents can prevent such hypertrophic responses in the heart. However, little is known regarding the roles of the calcineurin downstream effecter – nuclear factor of activated T cells. Our present study has further examined the roles of nuclear factor of activated T cells in pressure-overload cardiac hypertrophy by employing a recently developed cell-permeable nuclear factor of activated T cells inhibitor peptide. Rat hearts were subjected to pressure overload attributable by 4 weeks of aortic banding, and then treated with this cell-permeable nuclear factor of activated T cells inhibitor peptide and a control peptide. Treatment with the inhibitor was found to significantly decrease the heart weight/body weight ratio, the size of cardiac myocytes, and the serum brain natriuretic peptide and atrial natriuretic peptide levels. These results suggest that nuclear factor of activated T cells functions in a key role in the development of cardiac hypertrophy during pressure overload. Inhibition of nuclear factor of activated T cells by a specific inhibitor peptide is a suitable method for characterization of the molecular mechanisms underlying cardiac hypertrophy as well as in the search for new promising therapies for disease.
- Subjects
T cells; CARDIAC hypertrophy; CYCLOSPORINE; PEPTIDES; ATRIAL natriuretic peptides; THERAPEUTICS; PHARMACOLOGY
- Publication
Chemical Biology & Drug Design, 2006, Vol 67, Issue 3, p238
- ISSN
1747-0277
- Publication type
Article
- DOI
10.1111/j.1747-0285.2006.00360.x