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Poly(ADP-ribose) polymerase 2 contributes to neuroinflammation and neurological dysfunction in mouse experimental autoimmune encephalomyelitis

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dc.contributor.author Kamboj, Amit
dc.contributor.author Lu, Ping
dc.contributor.author Cossoy, Michael B
dc.contributor.author Stobart, Jillian L
dc.contributor.author Dolhun, Brian A
dc.contributor.author Kauppinen, Tiina M
dc.contributor.author de Murcia, Gilbert
dc.contributor.author Anderson, Christopher M
dc.date.accessioned 2013-05-01T15:04:45Z
dc.date.available 2013-05-01T15:04:45Z
dc.date.issued 2013-04-22
dc.identifier.citation Journal of Neuroinflammation. 2013 Apr 22;10(1):49
dc.identifier.uri http://hdl.handle.net/1993/19754
dc.description.abstract Abstract Background Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis characterized by entry of activated T cells and antigen presenting cells into the central nervous system and subsequent autoimmune destruction of nerve myelin. Previous studies revealed that non-selective inhibition of poly(ADP-ribose) polymerases (PARPs) 1 and 2 protect against neuroinflammation and motor dysfunction associated with EAE, but the role of the PARP-2 isoform has not yet been investigated selectively. Results EAE was induced in mice lacking PARP-2, and neurological EAE signs, blood-spine barrier (BSB) permeability, demyelination and inflammatory infiltration were monitored for 35 days after immunization. Mice lacking PARP-2 exhibited significantly reduced overall disease burden and peak neurological dysfunction. PARP-2 deletion also significantly delayed EAE onset and reduced BSB permeability, demyelination and central nervous system (CNS) markers of proinflammatory Th1 and Th17 T helper lymphocytes. Conclusions This study represents the first description of a significant role for PARP-2 in neuroinflammation and neurological dysfunction in EAE.
dc.title Poly(ADP-ribose) polymerase 2 contributes to neuroinflammation and neurological dysfunction in mouse experimental autoimmune encephalomyelitis
dc.type Journal Article
dc.language.rfc3066 en
dc.description.version Peer Reviewed
dc.rights.holder Amit Kamboj et al.; licensee BioMed Central Ltd.
dc.date.updated 2013-05-01T15:05:13Z
dc.identifier.doi http://dx.doi.org/10.1186/1742-2094-10-49


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