title: Expressions of C5a and its receptor CD88 after spinal cord injury in C3-deficient mice.
abstract: 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 C3 deficiency can reduce the secondary injury and improve the regeneration and functional recovery after SCI. However, recently, it was reported that C5a 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 C5a on neurons, it is necessary to study the expression profiles of C5a and its receptor CD88 after SCI and the influence on their expression when C3 was knocked out. By immunohistochemistry and Western blot, we found that in wild-type (WT) mice, both the expression of C5a and its receptor CD88 increased significantly, and there were two peaks during their expression after SCI. However, in C3-deficient mice, the expression of C5a still increased after SCI, although it was lower than that in WT group at every time points after SCI, and the expression of CD88 remained stable. Our study suggests that the expressions of C5a and CD88 can be inhibited in different degrees after SCI when the activation of complement system is blocked through C3 deficiency, which can reduce the secondary injury caused by C5a after SCI on one hand but deprive neurons of the possible protective effect from C5a on the other hand.
authors.affiliation: Department of Neurobiology, Chongqing Key Laboratory of Neurobiology, Third Military Medical University, Chongqing, China. guoqiang2005cq@yahoo.com.cn
authors.forename: Q
authors.initials: Q
authors.lastname: Guo
authors.forename: J
authors.initials: J
authors.lastname: Cheng
authors.forename: H
authors.initials: H
authors.lastname: Zhang
authors.forename: J
authors.initials: J
authors.lastname: Zhang
authors.forename: B
authors.initials: B
authors.lastname: Su
authors.forename: C
authors.initials: C
authors.lastname: Bian
authors.forename: S
authors.initials: S
authors.lastname: Lin
mesh_terms: D000818:Animals; D003176:Complement C3 / Q000172:deficiency* / Q000276:immunology; D015936:Complement C5a / Q000276:immunology / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D007150:Immunohistochemistry; D051379:Mice; D018345:Mice, Knockout; D044087:Receptor, Anaphylatoxin C5a / Q000276:immunology / Q000378:metabolism*; D013119:Spinal Cord Injuries / Q000276:immunology / Q000378:metabolism*; D013997:Time Factors
chemical_list: D003176:Complement C3; D044087:Receptor, Anaphylatoxin C5a; D015936:Complement C5a