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NF-B activation is required for the development of cardiac hypertrophy in vivo

Departments of ¹Surgery and ²Internal Medicine, East Tennessee State University, Johnson City, Tennessee 37614; and ³Department of Pathophysiology, Nanjing Medical University, and ⁴Animal Model Research Center, Nanjing University, Nanjing 210093, China

Submitted 12 February 2004 ; accepted in final form 23 April 2004

In the present study, we examined whether NF-B activation is required for cardiac hypertrophy in vivo. Cardiac hypertrophy in rats was induced by aortic banding for 1, 3, and 5 days and 1–6 wk, and age-matched sham-operated rats served as controls. In a separate group of rats, an IB- dominant negative mutant (IB-M), a superrepressor of NF-B activation, or pyrrolidinedithiocarbamate (PDTC), an antioxidant that can inhibit NF-B activation, was administered to aortic-banded rats for 3 wk. The heart weight-to-body weight ratio was significantly increased at 5 days after aortic banding, peaked at 4 wk, and remained elevated at 6 wk compared with age-matched sham controls. Atrial natriuretic peptide and brain natriuretic peptide mRNA expressions were significantly increased after 1 wk of aortic banding, reached a maximum between 2 and 3 wk, and remained increased at 6 wk compared with age-matched sham controls. NF-B activity was significantly increased at 1 day, reached a peak at 3 wk, and remained elevated at 6 wk, and IKK- activity was significantly increased at 1 day, peaked at 5 days, and then decreased but remained elevated at 6 wk after aortic banding compared with age-matched sham controls. Inhibiting NF-B activation in vivo by cardiac transfection of IB-M or by PDTC treatment significantly attenuated the development of cardiac hypertrophy in vivo with a concomitant decrease in NF-B activity. Our results suggest that NF-B activation is required for the development of cardiac hypertrophy in vivo and that NF-B could be an important target for inhibiting the development of cardiac hypertrophy in vivo.

myocardium; signal transduction; nuclear factor-B

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