IMR Press / FBL / Volume 14 / Issue 7 / DOI: 10.2741/3411

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Tollip attenuated the hypertrophic response of cardiomyocytes induced by IL-1beta
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1 Department of Pathophysiology, Nanjing Medical University, Nanjing, 210029, China
2 Department of Physiology, Xiangnan University, Chenzhou, 423043, China
3 Department of Surgery, East Tennessee State University, Johnson City, TN 37614, USA
4 Department of Internal Medicine, East Tennessee State University, Johnson City, TN 37614, USA
Academic Editor:Chuanfu Li
Front. Biosci. (Landmark Ed) 2009, 14(7), 2747–2756; https://doi.org/10.2741/3411
Published: 1 January 2009
Abstract

We examined the role of Tollip in the hypertrophic response of cardiomyocytes. C57BL/6 mice were subjected to transverse aortic constriction (TAC) for 2 weeks and age-matched sham surgical operated mice served as control. TAC significantly reduced the association of Tollip with IRAK-1 by 66.4 percent and increased NF-kappaB binding activity by 86.5 percent and the levels of phospho-p38 by 114.6 percent in the myocardium compared with sham control, respectively. In vitro experiments showed that IL-1beta stimulation also significantly reduced the association of Tollip with IRAK-1 and increased NF-kappaB binding activity in neonatal cardiomyocytes. Tollip overexpression by transfection of cardiac myocytes significantly attenuated the IL-1beta-induced hypertrophic response of cardiac myocytes as evidenced by reduced cell size (16.4 percent) and decreased ANP expression (33.3 percent). Overexpression of Tollip also reduced NF-kappaB binding activity by 30.7 percent and phospho-p38 by 47.1 percent, respectively. The results suggest that Tollip could be a negative regulator during the development of cardiac hypertrophy. The negative regulation of cardiac hypertrophy by Tollip may involve downregulation of the MyD88-dependent NF-kappaB activation pathway.

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