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Cardiovascular Research Advance Access [Accepted Manuscript] published online on June 1, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp180
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Liver X Receptors are negative regulators of cardiac hypertrophy via suppressing NF-{kappa}B signaling

Sijie Wu1,2,*, Ran Yin3,*, Rick Ernest4, Yuquan Li1, Olga Zhelyabovska1, Jinwen Luo1,2, Yifeng Yang2 and Qinglin Yang1,#

1 Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, AL
2 Xiangya Medical College, Zhongnan University, Changsha, China
3 Department of Cardiology, Jiangxi Medical College, Nanchang, China
4 Cardiovascular Research Institute, Morehouse School of Medicine, Atlanta, GA

# Corresponding should address to: Dr. Qinglin Yang, Department of Nutrition Sciences, University of Alabama at Birmingham, Webb 435, 1675 University Blvd, Birmingham, AL 35242. Phone: 205-996-6022; Fax: 205-934-7049; E-mail: qyang{at}uab.edu

Aims: Nuclear factor-{kappa}B (NF-{kappa}B) plays a critical role in cell growth and inflammation during the progression of cardiac hypertrophy and heart failure. Several members of nuclear receptor superfamily, including liver X receptors (LXR{alpha} and LXRβ), have been shown to suppress inflammatory responses, but little is known about their effects in cardiomyocytes.

Methods: We investigated LXR expression patterns in pressure overload-induced hypertrophic hearts and the hypertrophic growth of the LXR{alpha}-deficient hearts from mice (C57/B6) in response to pressure overload. The underlying mechanisms were also explored using cultured myocytes.

Results: We found that cardiac expression of LXR{alpha} was upregulated in pressure overload-induced left ventricular hypertrophy in mice. Transverse aorta coarctation-induced left ventricular hypertrophy was exacerbated in LXR{alpha}-null mice relative to control mice. A synthetic LXR ligand, T1317, suppressed cardiomyocyte hypertrophy in response to angiotensin II and lipopolysaccharide treatments. In addition, LXR activation suppressed NF-{kappa}B signalling and the expression of associated inflammatory factors. Overexpression of constitutively active LXR{alpha} and β in cultured myocytes suppressed NF-{kappa}B activity.

Conclusion: LXRs are negative regulators of cardiac growth and inflammation via suppressing NF-{kappa}B signaling in cardiomyocytes. This should provide new insights into novel therapeutic targets for treating cardiac hypertrophy and heart failure.

Time for primary review: 24 Days

* These authors contribute equally


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