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B ACTIVATION IS REQUIRED FOR THE DEVELOPMENT OF CARDIAC HYPERTROPHY IN VIVO
1 Department of Surgery, East Tennessee State University, Johnson City, TN, USA; Department of Pathophysiology, Nanjing Medical University, Nanjing, Jiangsu, China
2 Department of Surgery, East Tennessee State University, Johnson City, TN, USA
3 Animal Model Research Center, Nanjing University, Nanjing, Jiangsu, China
4 Department of Internal Medicine, East Tennessee State Univeristy, Johnson City, TN, USA
5 Department of Surgery, East Tennessee State University, Johnson City, TN, USA; Animal Model Research Center, Nanjing University, Nanjing, Jiangsu, China
* To whom correspondence should be addressed. E-mail: Li{at}ETSU.EDU.
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, 5 days and 1-6 weeks and age-matched sham operated rats served as controls. In a separate group of rats, IB
dominant negative mutant (IBM), a superrepressor of NFB activation, or pyrrolidinedithiocarbamate (PDTC), an antioxidant which can inhibit NFB activation, was administered to aortic banded rats for 3 weeks. The heart weight/body weight (HW/BW) ratio was significantly increased at 5 days following aortic banding, peaked at 4 weeks, and remained elevated at 6 weeks compared to age-matched sham controls. ANP and BNP mRNA expressions
were significantly increased after 1 week of aortic banding, reached a maximum between 2 and 3 weeks, and remained increased at 6 weeks compared to age-matched sham controls. NFB activity was significantly increased at 1 day, reached a peak at 3 weeks, and remained elevated at 6 weeks, and IKK
activity was significantly increased at 1 day, peaked at 5 days, then decreased but remained elevated at 6 weeks following aortic banding compared to age-matched sham controls. Inhibiting NFB activation in vivo by cardiac transfection of an IBM or by PDTC treatment significantly attenuated the development of cardiac hypertrophy in vivo with concomitant decrease in NFB activity. Our results suggest that NFB activation is required for
the development of cardiac hypertrophy in vivo and NFB could be an important target for inhibiting the development of cardiac hypertrophy in vivo.
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