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Poster Session 4Session Title: Oxidative Stress, Nitroso-redox Imbalance and Aging

Abstract P317: Acute Exercise Stress and ROS Signaling: Activation of Nrf2/ARE-Dependent Antioxidant Defense Mechanisms in the Mouse Myocardium

Corey J Miller, Kalavathy Ramachandran, Gayatri D Khanderao, Sankaranarayanan Kannan, Vasanthi Rajasekaran, Christoph Boheme, J David Symons, Christopher J Davidson, Rajasekaran Namakkal Soorappan
Circulation Research. 2011;109:AP317
Corey J Miller
Univ of Utah Health Care, Salt Lake City, UT
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Kalavathy Ramachandran
Univ of Utah Health Care, Salt Lake City, UT
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Gayatri D Khanderao
Univ of Utah Health Care, Salt Lake City, UT
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Sankaranarayanan Kannan
M D Anderson Cancer Cntr, Houston, TX
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Vasanthi Rajasekaran
Univ of Utah Health Care, Salt Lake City, UT
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Christoph Boheme
Univ of Utah, Salt Lake City, UT
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J David Symons
College of Exercise Physiology, Univ of Utah Health Care, Salt Lake City, UT
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Christopher J Davidson
Univ of Utah Health Care, Salt Lake City, UT
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Rajasekaran Namakkal Soorappan
Univ of Utah Sch of Medicine, Salt Lake City, UT
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Abstract

Background: Cellular defense mechanisms are crucial for maintaining intracellular redox state and mitigating free radical accumulation with aging. Nuclear Erythroid 2 p45 related factor-2 (Nrf2) regulates basal and inducible expression of numerous cytoprotective/antioxidant genes. We hypothesize that acute exercise will induce ROS, which triggers Nrf2/ARE signaling and promotes myocardial defense mechanisms.

Methods: Age-matched wild-type (WT) and Nrf2−/− (KO) mice at 2 and >20 months were subjected to acute exercise stress (AES) and then we assessed the activation of Nrf2/ARE-dependent transcriptional mechanisms in the heart. Myocardial ROS was measured by electron paramagnetic resonance (EPR) analysis.

Results: Under basal conditions, total ROS and GSH levels were identical at 2 months, whereas they were significantly impaired in Nrf2-KO when compared to Wt myocardium at ∼20 months indicating that Nrf2-deficiency is coupled with blemished redox potential. Upon AES, the young WT and KO mice exhibited oxidative stress (OS), but the WT were able compensate for the stress by increasing Nrf2 nuclear translocation and subsequent upregulation of cytoprotective genes. However, the aged (WT & KO) mice developed OS in response to AES. The degree of OS was several fold higher in the aged Nrf2-KO mice when compared with WT, suggesting an important age dependent function for Nrf2 in the myocardium. Western blot analysis revealed significant down regulation of major antioxidants (GCS, Nqo1, Ho1, catalase, G6pd and Gsr) in KO mice, while WT mice exhibited compensatory antioxidant response to the AES. Gene expression (qPCR) analysis revealed profound upregulation of major antioxidants in WT, but there was no such response occurred in KO mice after AES, suggesting Nrf2 independent mechanisms are inadequate to protect the myocardium.

Conclusions: Acute exercise induces ROS and thereby activates Nrf2 in the myocardium. However, disruption of Nrf2 increases susceptibility of the myocardium to OS induced damage. Thus Nrf2 signaling might be a potential therapeutic target to protect the heart from ROS and/or age dependent ischemia/reperfusion (I/R) injury and myocardial infarction (MI).

  • Aging
  • Oxidative stress
  • Exercise tests
  • © 2011 by American Heart Association, Inc.
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Circulation Research
9 December 2011, Volume 109, Issue Suppl 1
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    Abstract P317: Acute Exercise Stress and ROS Signaling: Activation of Nrf2/ARE-Dependent Antioxidant Defense Mechanisms in the Mouse Myocardium
    Corey J Miller, Kalavathy Ramachandran, Gayatri D Khanderao, Sankaranarayanan Kannan, Vasanthi Rajasekaran, Christoph Boheme, J David Symons, Christopher J Davidson and Rajasekaran Namakkal Soorappan
    Circulation Research. 2011;109:AP317, originally published October 8, 2015

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    Abstract P317: Acute Exercise Stress and ROS Signaling: Activation of Nrf2/ARE-Dependent Antioxidant Defense Mechanisms in the Mouse Myocardium
    Corey J Miller, Kalavathy Ramachandran, Gayatri D Khanderao, Sankaranarayanan Kannan, Vasanthi Rajasekaran, Christoph Boheme, J David Symons, Christopher J Davidson and Rajasekaran Namakkal Soorappan
    Circulation Research. 2011;109:AP317, originally published October 8, 2015
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