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Our previous study indicates that the interception of complement activation by <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>3 deficiency can reduce the secondary injury and improve the regeneration and functional recovery after <jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>. However, recently, it was reported that <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>5a which was generated during the complement activation pathways also had a protective effect on neurons, but whether it has the similar effect after <jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content> is unknown. To investigate the possibility and mechanism of the protective effect of <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>5a on neurons, it is necessary to study the expression profiles of <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>5a and its receptor <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>88 after <jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content> and the influence on their expression when <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>3 was knocked out. By immunohistochemistry and Western blot, we found that in wild\u2010type (WT) mice, both the expression of <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>5a and its receptor <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>88 increased significantly, and there were two peaks during their expression after <jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>. However, in <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>3\u2010deficient mice, the expression of <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>5a still increased after <jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>, although it was lower than that in WT group at every time points after <jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content>, and the expression of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>88 remained stable. Our study suggests that the expressions of <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>5a and <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>88 can be inhibited in different degrees after <jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content> when the activation of complement system is blocked through <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>3 deficiency, which can reduce the secondary injury caused by <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>5a after <jats:styled-content style=\"fixed-case\">SCI<\/jats:styled-content> on one hand but deprive neurons of the possible protective effect from <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>5a on the other hand.<\/jats:p>","DOI":"10.1111\/sji.12001","type":"journal-article","created":{"date-parts":[[2012,10,3]],"date-time":"2012-10-03T15:53:09Z","timestamp":1349279589000},"page":"224-229","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Expressions of <scp>C<\/scp>5a and Its Receptor <scp>CD<\/scp>88 After Spinal Cord Injury in <scp>C<\/scp>3\u2010deficient Mice"],"prefix":"10.1111","volume":"77","author":[{"given":"Q.","family":"Guo","sequence":"first","affiliation":[{"name":"Department of Neurobiology Chongqing Key Laboratory of Neurobiology Third Military Medical University Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Cheng","sequence":"additional","affiliation":[{"name":"Chongqing Normal University Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H.","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of 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