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Expressions of C 5a and Its Receptor CD 88 After Spinal Cord Injury in C 3‐deficient Mice
Author(s) -
Guo Q.,
Cheng J.,
Zhang H.,
Zhang J.,
Su B.,
Bian C.,
Lin S.
Publication year - 2013
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12001
Subject(s) - complement system , western blot , spinal cord injury , receptor , immunohistochemistry , chemistry , spinal cord , microbiology and biotechnology , immunology , medicine , neuroscience , biology , biochemistry , immune system , gene
The activation of complement system can aggravate the secondary injury after spinal cord injury ( SCI ). Our previous study indicates that the interception of complement activation by C 3 deficiency can reduce the secondary injury and improve the regeneration and functional recovery after SCI . However, recently, it was reported that C 5a which was generated during the complement activation pathways also had a protective effect on neurons, but whether it has the similar effect after SCI is unknown. To investigate the possibility and mechanism of the protective effect of C 5a on neurons, it is necessary to study the expression profiles of C 5a and its receptor CD 88 after SCI and the influence on their expression when C 3 was knocked out. By immunohistochemistry and Western blot, we found that in wild‐type (WT) mice, both the expression of C 5a and its receptor CD 88 increased significantly, and there were two peaks during their expression after SCI . However, in C 3‐deficient mice, the expression of C 5a still increased after SCI , although it was lower than that in WT group at every time points after SCI , and the expression of CD 88 remained stable. Our study suggests that the expressions of C 5a and CD 88 can be inhibited in different degrees after SCI when the activation of complement system is blocked through C 3 deficiency, which can reduce the secondary injury caused by C 5a after SCI on one hand but deprive neurons of the possible protective effect from C 5a on the other hand.