000101261 001__ 101261
000101261 005__ 20190527133823.0
000101261 0247_ $$2doi$$a10.1046/j.0953-816x.2001.01802.x
000101261 02470 $$2DAR$$a780
000101261 02470 $$a000172925900001$$2ISI
000101261 037__ $$aARTICLE
000101261 245__ $$aNeuroprotective effect of interleukin-6 and IL6/IL6R chimera in the quinolinic acid rat model of Huntington's syndrome
000101261 269__ $$a2001
000101261 260__ $$c2001
000101261 336__ $$aJournal Articles
000101261 500__ $$aDivision of Surgical Research and Gene Therapy Center, Lausanne Medical School, Pavillon 4, CHUV, 1011 Lausanne, Switzerland.
000101261 520__ $$aCiliary neurotrophic factor prevents behavioural deficits and striatal degeneration in rat and primate models of Huntington's disease. Interleukin- 6, another member of the cytokine family, and the chimeric molecule (IL6/IL6R) in which interleukin-6 and its soluble receptor are fused, have been shown to exert trophic action on various neuronal populations in the central nervous system. Therefore, we investigated the neuroprotective effect of these two molecules in the quinolinic acid model of Huntington's disease. LacZ-, interleukin-6- and IL6/IL6R-expressing lentiviral vectors were stereotaxically injected into the striatum of Wistar rats. Three weeks later the animals were lesioned through the intrastriatal injection of 180 nmol of quinolinic acid. The extent of the striatal damage was significantly diminished in the rats that had been treated with interleukin-6 or IL6/IL6R. The neuroprotective effect was, however, more pronounced with the IL6/IL6R chimera than with interleukin-6 as indicated by the volume of the lesions (38.6 +/- 10% in the IL6/IL6R group, 63.3 +/- 3.6% in the IL-6 group and 84.3 +/-2.9% in the control group). Quantitative analysis of striatal interneurons further demonstrated that the IL6/IL6R chimera is more neuroprotective than IL-6 on ChAT- and NADPH-d-immunoreactive neurons. These results suggest that the IL6/IL6R chimera is a potential treatment for Huntington's disease.
000101261 6531_ $$aAcetylcholine/metabolism
000101261 6531_ $$aAnimals
000101261 6531_ $$aDisease Models
000101261 6531_ $$aAnimal
000101261 6531_ $$aFemale
000101261 6531_ $$aGenetic Vectors/diagnostic use
000101261 6531_ $$aHuntington Disease/chemically induced/ drug therapy/physiopathology
000101261 6531_ $$aImmunohistochemistry
000101261 6531_ $$aInterleukin-6/genetics/metabolism/ pharmacology
000101261 6531_ $$aNeostriatum/ drug effects/metabolism/physiopathology
000101261 6531_ $$aNeurons/ drug effects/metabolism
000101261 6531_ $$aNeuroprotective Agents/ pharmacology
000101261 6531_ $$aQuinolinic Acid/pharmacology
000101261 6531_ $$aRats
000101261 6531_ $$aRats
000101261 6531_ $$aWistar
000101261 6531_ $$aReceptors
000101261 6531_ $$aInterleukin-6/ genetics/metabolism
000101261 6531_ $$aRecombinant Fusion Proteins/genetics/metabolism/ pharmacology
000101261 6531_ $$agamma-Aminobutyric Acid/metabolism
000101261 6531_ $$aAnimal
000101261 6531_ $$aRats
000101261 700__ $$0240445$$g150317$$aBensadoun, J.C.
000101261 700__ $$ade Almeida, L. P.
000101261 700__ $$aDreano, M.
000101261 700__ $$0240206$$g104359$$aAebischer, P.
000101261 700__ $$aDeglon, N.$$g150324$$0241685
000101261 773__ $$j14$$tEuropean Journal of Neuroscience$$k11$$q1753-61
000101261 909C0 $$xU10457$$0252067$$pLEN
000101261 909CO $$pSV$$particle$$ooai:infoscience.tind.io:101261
000101261 937__ $$aLEN-ARTICLE-2001-009
000101261 970__ $$a56/LEN
000101261 973__ $$rREVIEWED$$sPUBLISHED$$aEPFL
000101261 980__ $$aARTICLE