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Literature DB >> 20207017

Inhibition of C5a receptor alleviates experimental CNS lupus.

Alexander Jacob¹, Bradley Hack, Tao Bai, James R Brorson, Richard J Quigg, Jessy J Alexander.

Abstract

To investigate the role of C5a generated on complement activation in brain, the lupus model, MRL/lpr mice were treated with C5a receptor(R) antagonist (ant). Neutrophil infiltration, ICAM, TNF-alpha and iNOS mRNA expression, neuronal apoptosis and the expression of p-JNK, pSTAT1 and p-Erk were reduced and p-Akt increased on C5aR inhibition in MRL/lpr brains. MRL/lpr serum caused increased apoptosis in neurons showing that lupus had a direct effect on these cells. C5aRant pretreatment prevented the lupus serum induced loss of neuronal cells. Our findings demonstrate for the first time that C5a/C5aR signaling plays an important role in the pathogenesis of CNS lupus. Copyright 2010. Published by Elsevier B.V.

Entities: Chemical Disease Gene Species

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Year: 2010 PMID： 20207017 PMCID： PMC2902239 DOI： 10.1016/j.jneuroim.2010.02.011

Source DB: PubMed Journal: J Neuroimmunol ISSN： 0165-5728 Impact factor: 3.478

52 in total

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Journal: FASEB J Date: 2002-10 Impact factor: 5.191

8. Neurodegeneration in autoimmune MRL-lpr mice as revealed by Fluoro Jade B staining.

Authors: David A Ballok; Jason M Millward; Boris Sakic
Journal: Brain Res Date: 2003-02-28 Impact factor: 3.252

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Authors: Susanna H Weerth; Horea Rus; Moon L Shin; Cedric S Raine
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Review 10. Activation of complement in the central nervous system: roles in neurodegeneration and neuroprotection.

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4. CNS-specific expression of C3a and C5a exacerbate demyelination severity in the cuprizone model.

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5. C5a/CD88 signaling alters blood-brain barrier integrity in lupus through nuclear factor-κB.

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