Activation of the Nrf2–ARE pathway in muscle and spinal cord during ALS-like pathology in mice expressing mutant SOD1

Andrew D Kraft; Jon M Resch; Delinda A Johnson; Jeffrey A Johnson

doi:10.1016/j.expneurol.2007.05.026

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Activation of the Nrf2–ARE pathway in muscle and spinal cord during ALS-like pathology in mice expressing mutant SOD1

Journal article

Peer reviewed

Activation of the Nrf2–ARE pathway in muscle and spinal cord during ALS-like pathology in mice expressing mutant SOD1

Andrew D Kraft, Jon M Resch, Delinda A Johnson and Jeffrey A Johnson

Experimental neurology, Vol.207(1), pp.107-117

2007

DOI: 10.1016/j.expneurol.2007.05.026

PMCID: PMC2062571

PMID: 17631292

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Abstract

Oxidative stress plays a key role in the neuronal loss exhibited in amyotrophic lateral sclerosis (ALS), an event precipitating irreversible muscle atrophy. By crossing ALS mouse models (SOD G93A and SOD H46RH48Q) with an antioxidant response element (ARE) reporter mouse, we identified activation characteristics of the ARE system throughout the timecourse of motor neuron disease. Surprisingly, the earliest and most significant activation of this genetic sensor of oxidative stress occurred in the distal muscles of mutant SOD mice. The resultant data supports existing hypotheses that the muscle is somehow implicated during the initial pathology of these mice. Subsequently, Nrf2–ARE activation appears to progress in a retrograde fashion along the motor pathway. These data provide timely information concerning the contributions of the Nrf2–ARE pathway in ALS disease progression.

Oxidative Stress

Antioxidant response element (ARE)

Amyotrophic lateral sclerosis (ALS)

Neurodegeneration

Motor neuron disease

Superoxide dismutase (SOD)

Muscle

NFE2-related factor 2 (Nrf2)

Details

Title: Subtitle: Activation of the Nrf2–ARE pathway in muscle and spinal cord during ALS-like pathology in mice expressing mutant SOD1
Creators: Andrew D Kraft - Division of Pharmaceutical Sciences, Madison, WI, USA
Jon M Resch - Division of Pharmaceutical Sciences, Madison, WI, USA
Delinda A Johnson - Division of Pharmaceutical Sciences, Madison, WI, USA
Jeffrey A Johnson - Division of Pharmaceutical Sciences, Madison, WI, USA
Resource Type: Journal article
Publication Details: Experimental neurology, Vol.207(1), pp.107-117
DOI: 10.1016/j.expneurol.2007.05.026
PMID: 17631292
PMCID: PMC2062571
NLM abbreviation: Exp Neurol
ISSN: 0014-4886
eISSN: 1090-2430
Publisher: Elsevier Inc
Language: English
Date published: 2007
Academic Unit: Iowa Neuroscience Institute; Neuroscience and Pharmacology
Record Identifier: 9984065750502771

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