Deletion of UCP2 in iNOS deficient mice reduces the severity of the disease during experimental autoimmune encephalomyelitis.
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 chr...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2011-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3152556?pdf=render |
| _version_ | 1819290327052189696 |
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| author | Caroline Aheng Nathalie Ly Mairead Kelly Saleh Ibrahim Daniel Ricquier Marie-Clotilde Alves-Guerra Bruno Miroux |
| author_facet | Caroline Aheng Nathalie Ly Mairead Kelly Saleh Ibrahim Daniel Ricquier Marie-Clotilde Alves-Guerra Bruno Miroux |
| author_sort | Caroline Aheng |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-12-24T03:20:58Z |
| format | Article |
| id | doaj.art-17318dfede3c448a9334b8d3a4e40291 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-24T03:20:58Z |
| publishDate | 2011-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-17318dfede3c448a9334b8d3a4e402912022-12-21T17:17:30ZengPublic Library of Science (PLoS)PLoS ONE1932-62032011-01-0168e2284110.1371/journal.pone.0022841Deletion of UCP2 in iNOS deficient mice reduces the severity of the disease during experimental autoimmune encephalomyelitis.Caroline AhengNathalie LyMairead KellySaleh IbrahimDaniel RicquierMarie-Clotilde Alves-GuerraBruno MirouxUncoupling 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.http://europepmc.org/articles/PMC3152556?pdf=render |
| spellingShingle | Caroline Aheng Nathalie Ly Mairead Kelly Saleh Ibrahim Daniel Ricquier Marie-Clotilde Alves-Guerra Bruno Miroux Deletion of UCP2 in iNOS deficient mice reduces the severity of the disease during experimental autoimmune encephalomyelitis. PLoS ONE |
| title | Deletion of UCP2 in iNOS deficient mice reduces the severity of the disease during experimental autoimmune encephalomyelitis. |
| title_full | Deletion of UCP2 in iNOS deficient mice reduces the severity of the disease during experimental autoimmune encephalomyelitis. |
| title_fullStr | Deletion of UCP2 in iNOS deficient mice reduces the severity of the disease during experimental autoimmune encephalomyelitis. |
| title_full_unstemmed | Deletion of UCP2 in iNOS deficient mice reduces the severity of the disease during experimental autoimmune encephalomyelitis. |
| title_short | Deletion of UCP2 in iNOS deficient mice reduces the severity of the disease during experimental autoimmune encephalomyelitis. |
| title_sort | deletion of ucp2 in inos deficient mice reduces the severity of the disease during experimental autoimmune encephalomyelitis |
| url | http://europepmc.org/articles/PMC3152556?pdf=render |
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