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Int. J. Mol. Sci. 2017, 18(2), 245; doi:10.3390/ijms18020245

Identifying the Long-Term Role of Inducible Nitric Oxide Synthase after Contusive Spinal Cord Injury Using a Transgenic Mouse Model

1
The Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL 33136, USA
2
Department of Neurological Surgery, University of Virginia School of Medicine, Charlottesville, VA 22908, USA
3
Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institute of Heath, Bethesda, MD 20824, USA
4
Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA
5
Department of Neurological Surgery, University of Miami Miller School of Medicine, Miami, FL 33136, USA
6
Department of Genetics, Harvard Medical School, Boston, MA 02115, USA
7
The Neuroscience Program, University of Miami Miller School of Medicine, Miami, FL 33136, USA
8
The Interdisciplinary Stem Cell Institute, University of Miami Miller School of Medicine, Miami, FL 33136, USA
9
Department of Neurology, University of Miami Miller School of Medicine, Miami, FL 33136, USA
10
Department of Cell Biology and Anatomy, University of Miami Miller School of Medicine, Miami, FL 33136, USA
11
Bruce W. Carter Department of Veterans Affairs Medical Center, Miami, FL 33136, USA
*
Author to whom correspondence should be addressed.
Academic Editor: Katalin Prokai-Tatrai
Received: 5 December 2016 / Revised: 5 January 2017 / Accepted: 15 January 2017 / Published: 25 January 2017
(This article belongs to the Special Issue Neuroprotective Strategies 2016)
View Full-Text   |   Download PDF [2648 KB, uploaded 25 January 2017]   |  

Abstract

Inducible nitric oxide synthase (iNOS) is a potent mediator of oxidative stress during neuroinflammation triggered by neurotrauma or neurodegeneration. We previously demonstrated that acute iNOS inhibition attenuated iNOS levels and promoted neuroprotection and functional recovery after spinal cord injury (SCI). The present study investigated the effects of chronic iNOS ablation after SCI using inos-null mice. iNOS−/− knockout and wild-type (WT) control mice underwent a moderate thoracic (T8) contusive SCI. Locomotor function was assessed weekly, using the Basso Mouse Scale (BMS), and at the endpoint (six weeks), by footprint analysis. At the endpoint, the volume of preserved white and gray matter, as well as the number of dorsal column axons and perilesional blood vessels rostral to the injury, were quantified. At weeks two and three after SCI, iNOS−/− mice exhibited a significant locomotor improvement compared to WT controls, although a sustained improvement was not observed during later weeks. At the endpoint, iNOS−/− mice showed significantly less preserved white and gray matter, as well as fewer dorsal column axons and perilesional blood vessels, compared to WT controls. While short-term antagonism of iNOS provides histological and functional benefits, its long-term ablation after SCI may be deleterious, blocking protective or reparative processes important for angiogenesis and tissue preservation. View Full-Text
Keywords: oxidative stress; neuroprotection; angiogenesis; inducible nitric oxide synthase; knockout; axon; function oxidative stress; neuroprotection; angiogenesis; inducible nitric oxide synthase; knockout; axon; function
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Maggio, D.M.; Singh, A.; Iorgulescu, J.B.; Bleicher, D.H.; Ghosh, M.; Lopez, M.M.; Tuesta, L.M.; Flora, G.; Dietrich, W.D.; Pearse, D.D. Identifying the Long-Term Role of Inducible Nitric Oxide Synthase after Contusive Spinal Cord Injury Using a Transgenic Mouse Model. Int. J. Mol. Sci. 2017, 18, 245.

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