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- Title
Poly(ADP-ribose) polymerase 2 contributes to neuroinflammation and neurological dysfunction in mouse experimental autoimmune encephalomyelitis.
- Authors
Kamboj, Amit; Lu, Ping; Cossoy, Michael B; Stobart, Jillian L; Dolhun, Brian A; Kauppinen, Tiina M; de Murcia, Gilbert; Anderson, Christopher M
- Abstract
<bold>Background: </bold>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.<bold>Results: </bold>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.<bold>Conclusions: </bold>This study represents the first description of a significant role for PARP-2 in neuroinflammation and neurological dysfunction in EAE.
- Subjects
PERIPHERAL nervous system physiology; T cells; ANIMAL experimentation; DEMYELINATION; FLUORESCENT antibody technique; IMMUNITY; INFLAMMATION; MICE; NEUROLOGICAL disorders; RESEARCH funding; TRANSFERASES; DISEASE complications; PHYSIOLOGY
- Publication
Journal of Neuroinflammation, 2013, Vol 10, Issue 1, p49
- ISSN
1742-2094
- Publication type
journal article
- DOI
10.1186/1742-2094-10-49