Complement C6 deficiency exacerbates pathophysiology after spinal cord injury.

Autor: Su D; Department of Anatomy and Neurobiology, University of California, Irvine, Irvine, CA, USA., Hooshmand MJ; Department of Anatomy and Neurobiology, University of California, Irvine, Irvine, CA, USA.; Institute for Memory Impairments and Neurological Disorders (iMIND), University of California, Irvine, Irvine, CA, USA.; Sue and Bill Gross Stem Cell Research Center, University of California, Irvine, Irvine, CA, USA., Galvan MD; Department of Anatomy and Neurobiology, University of California, Irvine, Irvine, CA, USA., Nishi RA; Sue and Bill Gross Stem Cell Research Center, University of California, Irvine, Irvine, CA, USA., Cummings BJ; Department of Anatomy and Neurobiology, University of California, Irvine, Irvine, CA, USA.; Institute for Memory Impairments and Neurological Disorders (iMIND), University of California, Irvine, Irvine, CA, USA.; Sue and Bill Gross Stem Cell Research Center, University of California, Irvine, Irvine, CA, USA.; Department of Physical Medicine and Rehabilitation, University of California, Irvine, CA, USA., Anderson AJ; Department of Anatomy and Neurobiology, University of California, Irvine, Irvine, CA, USA. aja@uci.edu.; Institute for Memory Impairments and Neurological Disorders (iMIND), University of California, Irvine, Irvine, CA, USA. aja@uci.edu.; Sue and Bill Gross Stem Cell Research Center, University of California, Irvine, Irvine, CA, USA. aja@uci.edu.; Department of Physical Medicine and Rehabilitation, University of California, Irvine, CA, USA. aja@uci.edu.
Jazyk: angličtina
Zdroj: Scientific reports [Sci Rep] 2020 Nov 11; Vol. 10 (1), pp. 19500. Date of Electronic Publication: 2020 Nov 11.
DOI: 10.1038/s41598-020-76441-3
Abstrakt: Historically, the membrane attack complex, composed of complement components C5b-9, has been connected to lytic cell death and implicated in secondary injury after a CNS insult. However, studies to date have utilized either non-littermate control rat models, or mouse models that lack significant C5b-9 activity. To investigate what role C5b-9 plays in spinal cord injury and recovery, we generated littermate PVG C6 wildtype and deficient rats and tested functional and histological recovery after moderate contusion injury using the Infinite Horizon Impactor. We compare the effect of C6 deficiency on recovery of locomotor function and histological injury parameters in PVG rats under two conditions: (1) animals maintained as separate C6 WT and C6-D homozygous colonies; and (2) establishment of a heterozygous colony to generate C6 WT and C6-D littermate controls. The results suggest that maintenance of separate homozygous colonies is inadequate for testing the effect of C6 deficiency on locomotor and histological recovery after SCI, and highlight the importance of using littermate controls in studies involving genetic manipulation of the complement cascade.
Databáze: MEDLINE
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