Literature DB >> 21245055

Up-regulation of p27(kip1) contributes to Nrf2-mediated protection against angiotensin II-induced cardiac hypertrophy.

Jinqing Li1, Cheng Zhang, Yifan Xing, Joseph S Janicki, Masayuki Yamamoto, Xing Li Wang, Dong-Qi Tang, Taixing Cui.   

Abstract

AIMS: Nuclear factor erythroid-2-related factor 2 (Nrf2) appears to be a negative regulator of maladaptive cardiac remodelling and dysfunction; however, a potential of the Nrf2-mediated cardiac protection in diverse pathological settings remains to be determined. This study was aimed to explore the role of Nrf2 in angiotensin II (Ang II)-induced cardiac hypertrophy. METHODS AND
RESULTS: Littermate wild-type (WT) and Nrf2 knockout (Nrf2(-/-)) mice were administered Ang II via osmotic mini-pumps for 2 weeks to induce cardiac hypertrophy. Elevation of blood pressure by the continuous Ang II infusion was comparable between WT and Nrf2(-/-) mice. Relative to WT mice, however, Nrf2(-/-) mice exhibited exaggerated myocardial oxidative stress with an impaired induction of a group of antioxidant genes and increased cardiac hypertrophy in response to the sustained Ang II stimulation. In cultured cardiomyocytes, adenoviral overexpression of Nrf2 shRNA enhanced Ang II-induced reactive oxygen species (ROS) production and protein synthesis, whereas adenoviral overexpression of Nrf2 exerted opposite effects. Moreover, Nrf2 deficiency exacerbated Ang II-induced down-regulation of p27(kip1) expression in the heart via a mechanism of post-transcriptional regulation. In contrast, adenoviral overexpression of Nrf2 increased p27(kip1) protein but not mRNA expression and reversed Ang II-induced down-regulation of p27(kip1) protein expression in cultured cardiomyocytes by suppressing ROS formation. Finally, the enhancement of Ang II-induced hypertrophic growth due to the Nrf2 deficiency was negated by overexpressing p27(kip1) in cultured cardiomyocytes.
CONCLUSION: The Nrf2-p27(kip1) pathway serves as a novel negative feedback mechanism in Ang II-induced pathogenesis of cardiac hypertrophy, independent of changes in blood pressure.

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Year:  2011        PMID: 21245055     DOI: 10.1093/cvr/cvr010

Source DB:  PubMed          Journal:  Cardiovasc Res        ISSN: 0008-6363            Impact factor:   10.787


  40 in total

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Authors:  Qin M Chen; Anthony J Maltagliati
Journal:  Physiol Genomics       Date:  2017-11-29       Impact factor: 3.107

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4.  Role of nuclear factor erythroid 2-related factor 2 in the oxidative stress-dependent hypertension associated with the depletion of DJ-1.

Authors:  Santiago Cuevas; Yu Yang; Prasad Konkalmatt; Laureano D Asico; Jun Feranil; John Jones; Van Anthony Villar; Ines Armando; Pedro A Jose
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6.  New take on the role of angiotensin II in cardiac hypertrophy and fibrosis.

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Journal:  Hypertension       Date:  2011-04-18       Impact factor: 10.190

7.  Nrf2-Mediated Cardiac Maladaptive Remodeling and Dysfunction in a Setting of Autophagy Insufficiency.

Authors:  Qingyun Qin; Chen Qu; Ting Niu; Huimei Zang; Lei Qi; Linmao Lyu; Xuejun Wang; Mitzi Nagarkatti; Prakash Nagarkatti; Joseph S Janicki; Xing Li Wang; Taixing Cui
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Authors:  Wenjuan Wang; Siying Li; Hui Wang; Bin Li; Lei Shao; Yimu Lai; Gary Horvath; Qian Wang; Masayuki Yamamoto; Joseph S Janicki; Xing Li Wang; Dongqi Tang; Taixing Cui
Journal:  J Mol Cell Cardiol       Date:  2014-04-18       Impact factor: 5.000

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Authors:  Ying Huang; Wenji Li; Zheng-yuan Su; Ah-Ng Tony Kong
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10.  DL-3-n-butylphthalide improves ventricular function, and prevents ventricular remodeling and arrhythmias in post-MI rats.

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Journal:  Naunyn Schmiedebergs Arch Pharmacol       Date:  2018-03-30       Impact factor: 3.000

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