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dc.contributor.authorVillagra, Nuria T.-
dc.contributor.authorBerciano, José-
dc.contributor.authorAltable, Marcos-
dc.contributor.authorNavascués, Joaquín-
dc.contributor.authorCasafont, Íñigo-
dc.contributor.authorLafarga, Miguel-
dc.contributor.authorBerciano, María T.-
dc.identifierdoi: 10.1016/j.nbd.2004.02.005-
dc.identifierissn: 0969-9961-
dc.identifier.citationNeurobiology of Disease 16(1): 158-168 (2004)-
dc.description.abstractAcute inflammatory demyelinating polyneuropathy (AIDP) is a type of Guillain-Barré syndrome (GBS) characterized by primary nerve demyelination sometimes with secondary axonal degeneration. Studies on the fine structure of dorsal root ganglia in AIDP are lacking. Our aim was to investigate the cytology and nuclear organization of primary sensory neurons in AIDP with axonal injury using ultrastructural and immunohistochemical analysis. The light cytology of the L5 dorsal ganglion showed the characteristic findings of neuronal axonal reaction. The organization of chromatin, nucleolus, Cajal bodies, and nuclear pores corresponded to transcriptionally active neurons. However, the hallmark of the nuclear response to axonal injury was the formation of numerous nuclear bodies (NBs; 6.37 ± 0.6, in the AIDP, vs. 2.53 ± 0.2, in the control, mean ± SDM), identified as promyelocytic leukemia (PML) bodies by the presence of the protein PML. In addition to PML protein, nuclear bodies contained SUMO-1 and the transcriptional regulators CREB-binding protein (CBP) and glucocorticoid receptor (GR). The presence of proteasome 19S was also detected in some nuclear bodies. We suggest that neuronal PML bodies could regulate the nuclear concentration of active proteins, a process mediated by protein interactions with PML and SUMO-1 proteins. In the AIDP case, the proliferation of PML bodies may result from the overexpression of some nuclear proteins due to changes in gene expression associated with axonal injury. © 2004 Elsevier Inc. All rights reserved.-
dc.description.sponsorshipThis work was supported by the following grants: “Centro de Investigación de Enfermedades Neurológicas (CIEN)”, “Instituto de Salud Carlos III (Madrid, Spain)”; “Dirección General de Investigacion” from Spain (BFI2002-0454); and “Fundación Marqués de Valdecilla” (A04/03) from Santander, Spain.-
dc.titlePML bodies in reactive sensory ganglion neurons of the Guillain- Barré syndrome-
dc.description.versionPeer Reviewed-
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