期刊
CIRCULATION
卷 101, 期 20, 页码 2431-2437出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.CIR.101.20.2431
关键词
aorta; hypertrophy; pressure
资金
- NHLBI NIH HHS [HL-69562] Funding Source: Medline
- NIEHS NIH HHS [T32 ES07051] Funding Source: Medline
Background-Vascular hypertension resulting in increased cardiac load is associated with left ventricular hypertrophy and is a leading predicator for progressive heart disease. The molecular signaling pathways that respond to increases in cardiac load are poorly understood. One potential regulator of the hypertrophic response is the calcium-sensitive phosphatase calcineurin. Methods and Results-We showed that calcineurin enzymatic activity is increased 3.2-fold in the heart in response to pressure-overload hypertrophy induced by abdominal aortic banding in the rat. Western blot analysis further demonstrates that calcineurin A (catalytic subunit) protein content and association with calmodulin are increased in response to pressure-overload hypertrophy. This increase in calcineurin protein content was prevented by administration of the calcineurin inhibitor cyclosporine A (CsA), CsA administration attenuated load-induced cardiac hypertrophy in a dose-dependent manner over a 14-day treatment protocol. CsA administration also partially reversed pressure-overload hypertrophy in aortic-banded rats after 14 days. CsA also attenuated the histological and molecular indexes of pressure-overload hypertrophy. Conclusions-These data suggest that calcineurin is an important upstream regulator of load-induced hypertrophy.
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