RGD Reference Report - Deletion of UCP2 in iNOS deficient mice reduces the severity of the disease during experimental autoimmune encephalomyelitis. - Rat Genome Database

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Deletion of UCP2 in iNOS deficient mice reduces the severity of the disease during experimental autoimmune encephalomyelitis.

Authors: Aheng, C  Ly, N  Kelly, M  Ibrahim, S  Ricquier, D  Alves-Guerra, MC  Miroux, B 
Citation: Aheng C, etal., PLoS One. 2011;6(8):e22841. Epub 2011 Aug 8.
RGD ID: 5509069
Pubmed: PMID:21857957   (View Abstract at PubMed)
PMCID: PMC3152556   (View Article at PubMed Central)
DOI: DOI:10.1371/journal.pone.0022841   (Journal Full-text)

Uncoupling protein 2 is a member of the mitochondrial anion carrier family that is widely expressed in neurons and the immune cells of humans. Deletion of Ucp2 gene in mice pre-activates the immune system leading to higher resistance toward infection and to an increased susceptibility to develop chronic inflammatory diseases as previously exemplified with the Experimental Autoimmune Encephalomyelitis (EAE), a mouse model for multiple sclerosis. Given that oxidative stress is enhanced in Ucp2-/- mice and that nitric oxide (NO) also plays a critical function in redox balance and in chronic inflammation, we generated mice deficient for both Ucp2 and iNos genes and submitted them to EAE. Mice lacking iNos gene exhibited the highest clinical score (3.4+/-0.5 p<0.05). Surprisingly, mice deficient for both genes developed milder disease with reduced immune cell infiltration, cytokines and ROS production as compared to iNos-/- mice.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Experimental Autoimmune Encephalomyelitis  ISONos2 (Mus musculus)5509069; 5509069 RGD 
Experimental Autoimmune Encephalomyelitis  IMP 5509069 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Nos2  (nitric oxide synthase 2)

Genes (Mus musculus)
Nos2  (nitric oxide synthase 2, inducible)

Genes (Homo sapiens)
NOS2  (nitric oxide synthase 2)


Additional Information