Uncoupling Protein 2
Posted: Wed May 03, 2006 6:57 am
Uncoupleing Protein 2 is a new one on me. It looks interesting because it is involved in neuroprotection AND plays a role in insulin secretion.
Uncoupling Protein 2 Has Protective Function during Experimental Autoimmune Encephalomyelitis.
Am J Pathol. 2006 May;168(5):1570-1575.
Vogler S, Pahnke J, Rousset S, Ricquier D, Moch H, Miroux B, Ibrahim SM.
M.D. Institute of Immunology, University of Rostock, Schillingallee 70, 18055 Rostock, Germany; or to Bruno Miroux, Ph.D., BioTram, CNRS UPR9078, Faculte de Medecine Necker Enfants Malades, 156 rue de Vaugirard, 75730 Paris Cedex 15, France. saleh.ibrahim@med.uni-rostock.de.
Uncoupling protein 2 (UCP2) is a member of the mitochondrial transporter superfamily that is expressed in many tissues, including immune cells. UCP2 prevents oxidative stress by reducing reactive oxygen species. Using UCP2-deficient mice, it was shown that UCP2 is involved in the regulation of insulin secretion, in the resistance to infection, and in atherosclerosis.
Here, we investigated the role of UCP2 in experimental autoimmune encephalomyelitis, a murine model of multiple sclerosis. Immunized C57BL/6J UCP2-deficient mice showed a slightly delayed onset during experimental autoimmune encephalomyelitis (13.0 +/- 0.6 versus 11.5 +/- 0.8 in wild-type controls) and developed significantly higher disease scores than littermate controls (maximum disease score of 2.9 +/- 0.2 versus 1.7 +/- 0.2, P = 0.001). Higher levels of infiltrating T cells into the spinal cord meninges and parenchyma were observed. The T-cell proliferative response to the specific antigen was increased in UCP2-deficient mice compared with littermate controls, and CD4 cells of UCP2 knockout mice produced significantly higher levels of pro-inflammatory cytokines, eg, tumor necrosis factor-alpha and interleukin-2, resulting from a Th1 response. Mice lacking UCP2 also developed a higher B-cell response. Concomitantly, CD4 and CD8 cells of the UCP2-deficient mice showed increased production of reactive oxygen species.
These results suggest a protective function of UCP2 in chronic inflammatory diseases such as multiple sclerosis.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum
Uncoupling Protein 2 Has Protective Function during Experimental Autoimmune Encephalomyelitis.
Am J Pathol. 2006 May;168(5):1570-1575.
Vogler S, Pahnke J, Rousset S, Ricquier D, Moch H, Miroux B, Ibrahim SM.
M.D. Institute of Immunology, University of Rostock, Schillingallee 70, 18055 Rostock, Germany; or to Bruno Miroux, Ph.D., BioTram, CNRS UPR9078, Faculte de Medecine Necker Enfants Malades, 156 rue de Vaugirard, 75730 Paris Cedex 15, France. saleh.ibrahim@med.uni-rostock.de.
Uncoupling protein 2 (UCP2) is a member of the mitochondrial transporter superfamily that is expressed in many tissues, including immune cells. UCP2 prevents oxidative stress by reducing reactive oxygen species. Using UCP2-deficient mice, it was shown that UCP2 is involved in the regulation of insulin secretion, in the resistance to infection, and in atherosclerosis.
Here, we investigated the role of UCP2 in experimental autoimmune encephalomyelitis, a murine model of multiple sclerosis. Immunized C57BL/6J UCP2-deficient mice showed a slightly delayed onset during experimental autoimmune encephalomyelitis (13.0 +/- 0.6 versus 11.5 +/- 0.8 in wild-type controls) and developed significantly higher disease scores than littermate controls (maximum disease score of 2.9 +/- 0.2 versus 1.7 +/- 0.2, P = 0.001). Higher levels of infiltrating T cells into the spinal cord meninges and parenchyma were observed. The T-cell proliferative response to the specific antigen was increased in UCP2-deficient mice compared with littermate controls, and CD4 cells of UCP2 knockout mice produced significantly higher levels of pro-inflammatory cytokines, eg, tumor necrosis factor-alpha and interleukin-2, resulting from a Th1 response. Mice lacking UCP2 also developed a higher B-cell response. Concomitantly, CD4 and CD8 cells of the UCP2-deficient mice showed increased production of reactive oxygen species.
These results suggest a protective function of UCP2 in chronic inflammatory diseases such as multiple sclerosis.
http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum