The alternative receptor for complement component 5a, C5aR2, conveys neuroprotection in traumatic spinal cord injury

Biggins, Patrick, Brennan, Faith, Taylor, Stephen, Woodruff, Trent and Ruitenberg, Marc (2017) The alternative receptor for complement component 5a, C5aR2, conveys neuroprotection in traumatic spinal cord injury. Journal of Neurotrauma, 34 12: 2075-2085. doi:10.1089/neu.2016.4701

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Author Biggins, Patrick
Brennan, Faith
Taylor, Stephen
Woodruff, Trent
Ruitenberg, Marc
Title The alternative receptor for complement component 5a, C5aR2, conveys neuroprotection in traumatic spinal cord injury
Journal name Journal of Neurotrauma   Check publisher's open access policy
ISSN 0897-7151
1557-9042
Publication date 2017-04-26
Year available 2017
Sub-type Article (original research)
DOI 10.1089/neu.2016.4701
Open Access Status File (Author Post-print)
Volume 34
Issue 12
Start page 2075
End page 2085
Total pages 11
Place of publication New Rochelle, NY United States
Publisher Mary Ann Liebert, Inc. Publishers
Language eng
Formatted abstract
This study investigated the role of the alternative receptor for complement activation fragment C5a, C5aR2, in secondary inflammatory pathology after contusive spinal cord injury (SCI) in mice. C5ar2–/– mice exhibited decreased intraparenchymal tumor necrosis factor alpha and interleukin-6 acutely post-injury, but these reductions did not translate into improved outcomes. We show that loss of C5aR2 leads to increased lesion volumes, reduced myelin sparing, and significantly worsened recovery from SCI in C5ar2–/– animals compared to wild-type (WT) controls. Loss of C5aR2 did not alter leukocyte mobilization from the bone marrow in response to SCI, and neutrophil recruitment/presence at the lesion site was also not different between genotypes. Acute treatment of SCI mice with the selective C5aR1 antagonist, PMX205, improved SCI outcomes, compared to vehicle controls, and, importantly, fully alleviated the worsened recovery of C5ar2–/– mice compared to their WT counterparts. Collectively, these findings indicate that C5aR2 is neuroprotective and a novel target to restrain injurious C5a signaling after a major neurotraumatic event.
Keyword Ddegeneration
Inflammation
Neural injury
Secondary insult
Traumatic spinal cord injury
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

 
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Created: Thu, 18 May 2017, 15:27:17 EST by Kirstie Asmussen on behalf of Queensland Brain Institute