NDLI: Immunosuppressant FK506 enhances phosphorylation of nitric oxide synthase and protects against glutamate neurotoxicity.

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Immunosuppressant FK506 enhances phosphorylation of nitric oxide synthase and protects against glutamate neurotoxicity.

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Immunosuppressant FK506 enhances phosphorylation of nitric oxide synthase and protects against glutamate neurotoxicity.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Dawson, V. L. Dawson, T. M. Uhl, G. R. Dinerman, J. L. Steiner, J. P. Snyder, S. H.
Description	Author Affiliation: Dawson TM ( Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205.);
Abstract	Immunosuppressants FK506 and cyclosporin A inhibit neurotoxicity of N-methyl-D-aspartate in primary cortical cultures, while having no effect on quisqualate- and kainate-mediated neurotoxicity. Rapamycin completely reverses the neuroprotective effect of FK506. Both FK506 and cyclosporin A inhibit NMDA-elicited/nitric oxide-mediated increases in cGMP levels in cortical cultures. FK506 has no effect on sodium nitroprusside-induced increases in cGMP. In a stably transfected human kidney 293 cell line overexpressing the gene encoding nitric oxide synthase [L-arginine, NADPH:oxygen oxidoreductase (nitric oxide-forming), EC 1.14.13.39], FK506 inhibits the calcium ionophore A23187, stimulated increases in nitrite (a breakdown product of nitric oxide), and potentiates phorbol ester-mediated inhibition of nitrite formation. FK506-mediated inhibition of nitric oxide formation is completely reversed by rapamycin. Calcineurin dephosphorylates protein kinase C-mediated phosphorylation of nitric oxide synthase. FK506 prevents the calcineurin-mediated dephosphorylation of nitric oxide synthase and thereby diminishes the enzyme's catalytic activity. These data establish nitric oxide synthase as a calcineurin substrate. Nitric oxide synthase catalytic activity is regulated by the phosphorylation state of the enzyme. Enhanced phosphorylation of nitric oxide synthase diminishes catalytic activity, and dephosphorylation (through activation of calcineurin) enhances catalytic activity. The neuroprotective effect of FK506 and cyclosporin A presumably involves the inhibition of calcineurin, preventing the dephosphorylation of nitric oxide synthase and its subsequent activation.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	21
Volume Number	90
Language	English
Publisher	National Academy of Sciences
Publisher Date	1993-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Amino Acid Oxidoreductases Metabolism Cell Death Drug Effects Cerebral Cortex Glutamates Toxicity Neurons Neurotoxins Tacrolimus Pharmacology Antagonists & Inhibitors Animals Cells, Cultured Cytology Enzymology Excitatory Amino Acid Antagonists Fetus Glutamic Acid Immunosuppressive Agents N-Methylaspartate Nitric Oxide Synthase Phosphorylation Polyenes Rats, Sprague-Dawley Sirolimus Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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