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Ahmad AS, Shah ZA, Doré S. Protective Role of Arginase II in Cerebral Ischemia and Excitotoxicity. J Neurol Neurosci. 2016;7(2)doi: 10.21767/2171-6625.100088.
Ahmad, A. S., Shah, Z. A., & Doré, S. (2016). Protective Role of Arginase II in Cerebral Ischemia and Excitotoxicity. Journal of neurology and neuroscience, 7(2), . https://doi.org/10.21767/2171-6625.100088
Ahmad, Abdullah Shafique, et al. "Protective Role of Arginase II in Cerebral Ischemia and Excitotoxicity." Journal of neurology and neuroscience vol. 7,2 (2016). doi: https://doi.org/10.21767/2171-6625.100088
Ahmad AS, Shah ZA, Doré S. Protective Role of Arginase II in Cerebral Ischemia and Excitotoxicity. J Neurol Neurosci. 2016;7(2). doi: 10.21767/2171-6625.100088. Epub 2016 Apr 29. PMID: 27308186; PMCID: PMC4905713.
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J Neurol Neurosci. 2016;7(2). doi: 10.21767/2171-6625.100088. Epub 2016 Apr 29.

Protective Role of Arginase II in Cerebral Ischemia and Excitotoxicity.

Journal of neurology and neuroscience

Abdullah Shafique Ahmad, Zahoor Ahmad Shah, Sylvain Doré

Affiliations

  1. Department of Anesthesiology, University of Florida, Gainesville, 32610, FL, USA; Center for Translational Research in Neurodegenerative Disease, University of Florida, Gainesville, 32610, FL, USA.
  2. Department of Medicinal and Biological Chemistry, University of Toledo, Toledo 43614, OH, USA.
  3. Department of Anesthesiology, University of Florida, Gainesville, 32610, FL, USA; Center for Translational Research in Neurodegenerative Disease, University of Florida, Gainesville, 32610, FL, USA; Departments of Neurology, Psychiatry, Psychology, Pharmaceutics, and Neuroscience, University of Florida, Gainesville, 32610 FL, USA.

PMID: 27308186 PMCID: PMC4905713 DOI: 10.21767/2171-6625.100088

Abstract

BACKGROUND: Arginase (Arg), one of the enzymes involved in the urea cycle, provides an essential route for the disposal of excess nitrogen resulting from amino acid and nucleotide metabolism. Two reported subtypes of Arg (ArgI and II) compete with nitric oxide synthase (NOS) to use L-arginine as a substrate, and subsequently regulate NOS activity. It has been reported that Arg has significant effects on circulation that suggest the potential role of this enzyme in regulating vascular function. However, the role of Arg following brain damage has not been elucidated. In this study, we hypothesize that the deletion of ArgII will lead to aggravated brain injury following cerebral ischemia and excitotoxicity.

METHODS AND FINDINGS: To test our hypothesis, male C57BL/6 wildtype (WT) and ArgII

CONCLUSION: Targeting ArgII could be considered an integrative part of a multi-modal approach to fight acute brain damage excitotoxicity, ischemic brain injury, and other forms of brain trauma.

Keywords: Cerebral blood flow; Mice; NMDA; Neuroprotection; Nitric oxide synthase; Stroke; Vasodilation

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