Activation of the complement cascade and increase of clusterin in the brain following a cortical contusion in the adult rat.
The aim of the present study was to examine the glial cell response and the possible involvement of the complement cascade following a cerebral cortical contusion. The lesion was produced using a standardized weight-drop technique in adult rats. The blood-brain barrier was damaged, as demonstrated by a decrease of immunoreactivity for a tight junction protein normally expressed by endothelial cells of small vessels in the central nervous system. Increased immunoreactivity for microglial (OX42) and astroglial cells (glial fibrillary acidic protein), as well as macrophages expressing ED1-immunoreactivity (IR) were found in the vicinity of the lesion at all postoperative survival times (2-14 days). In the present study complement factor C3d- and C9-IR was found around the lesion, indicating that activation of the complement cascade had taken place. Furthermore, immunoreactivity for the putative complement inhibitor clusterin (sulfated glycoprotein-2) was found in some of the injured neurons. The contralateral hemisphere showed no evidence of the reaction found in the ipsilateral hemisphere. The balance between complement activation and complement inhibitors may have an impact on the degenerative components in the brain following traumatic injury and in particular on the events leading to nerve cell death.
Bellander
B M
BM
Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
von Holst
H
H
Fredman
P
P
Svensson
M
M
D000818:Animals; D001924:Brain Concussion / Q000378:metabolism*; D051152:Clusterin; D003169:Complement Inactivator Proteins / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D006023:Glycoproteins / Q000378:metabolism*; D007150:Immunohistochemistry; D018832:Molecular Chaperones; D051381:Rats; D017207:Rats, Sprague-Dawley
D051152:Clusterin; D003169:Complement Inactivator Proteins; D006023:Glycoproteins; D018832:Molecular Chaperones