GSNO attenuates EAE disease by S-nitrosylation-mediated modulation of endothelial-monocyte interactions.

GSNO attenuates EAE disease by S-nitrosylation-mediated modulation of endothelial-monocyte interactions. Research Abstract Details 

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GSNO attenuates EAE disease by S-nitrosylation-mediated modulation of endothelial-monocyte interactions. Abstract Text:

Ratna Prasad,Shailendra Giri,Narender Nath,Inderjit Singh,Avtar K Singh,

S-Nitrosoglutathione (GSNO) is an endogenous nitric oxide carrier and recently, has been documented for its anti-inflammatory effects in rat model of cerebral ischemia (Khan et al. (2005) J Cereb Blood Flow Metab 25:177-192). Here, we explored the neuroprotective effects mediated by GSNO in Lewis rat model of EAE and its mechanism of action using in vitro model of monocyte-endothelial cell interaction. Oral administration of GSNO attenuated the clinical disease course in EAE animals by inhibiting the infiltration of vascular immune cells in the CNS that subsequently led to the reduction in the expression of proinflammatory cytokines and consequently limited demyelination. Based on the inhibition in infiltration of immune cells, we hypothesized that GSNO modulated endothelial cell activation that led to reduce cellular infiltration in the CNS. Using an in vitro model, we established that GSNO inhibited monocyte adhesion to the activated endothelial cell, which was mediated by down regulation of endothelial cell adhesion molecules (CAMs). The mechanism by which GSNO modulated CAMs expression appeared to be via S-nitrosylation of p65, which consequently inhibited nuclear factor kappa B (NF-kappaB) activation in endothelial cells. These observations suggest that GSNO exerts its protective effects in EAE by inhibition of cellular infiltration into the CNS by S-nitrosylation of p65, thereby modulating NF-kappaB-CAMs pathway in endothelial cells.

GSNO attenuates EAE disease by S-nitrosylation-mediated modulation of endothelial-monocyte interactions. Publishing Authors By Initials

R Prasad,S Giri,N Nath,I Singh,AK Singh,

For similar peptides: intercellular signaling peptides and proteins: cytokines: monokines: tumor necrosis factor-alpha research abstracts see: peptides: intercellular signaling peptides and proteins: cytokines: monokines: tumor necrosis factor-alpha research

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GSNO attenuates EAE disease by S-nitrosylation-mediated modulation of endothelial-monocyte interactions. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Glia

VOLUME: 55

Page Numbers: 65-77

Journal Abbreviation: Glia

ISSN: 0894-1491

DAY: 1

MONTH: Jan

YEAR: 2007

GSNO attenuates EAE disease by S-nitrosylation-mediated modulation of endothelial-monocyte interactions. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8806785

GSNO attenuates EAE disease by S-nitrosylation-mediated modulation of endothelial-monocyte interactions. Keywords Mesh Terms:

KEYWORDS: Tumor Necrosis Factor-alpha

MESH TERMS: metabolism

Chemical & Substance for Abstract: GSNO attenuates EAE disease by S-nitrosylation-mediated modulation of endothelial-monocyte interactions. Information

Substance Name: S-Nitrosoglutathione

Registry Number: 57564-91-7

Grant and Affiliation Information for GSNO attenuates EAE disease by S-nitrosylation-mediated modulation of endothelial-monocyte interactions.

AFFILIATION: Department of Pediatrics, Medical University of South Carolina, Charleston, South Carolina 29425, USA.

Country: United States

AGENCY: United States NINDS

GRANT: NS-40810

ACRONYM: NS

MEDLINETA: Glia

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