Central nervous system-targeted complement inhibition mediates neuroprotection after closed head injury in transgenic mice.
The role of intracerebral complement activation after traumatic brain injury remains unclear. In this study, the authors demonstrate that transgenic mice with astrocyte-targeted expression of the soluble complement inhibitor sCrry have a significantly reduced neurologic impairment and improved blood-brain barrier function after closed head injury compared with wild-type C57BL/6 littermates. This work further implicates the complement system as a participant in secondary progression of brain damage after head trauma and provides a strong rationale for future studies of posttraumatic pharmacologic complement inhibition.
Rancan
Mario
M
Department of Trauma Surgery, The Alfred Hospital and Monash University, Melbourne, Victoria, Australia.
Morganti-Kossmann
Maria C
MC
Barnum
Scott R
SR
Saft
Silvia
S
Schmidt
Oliver I
OI
Ertel
Wolfgang
W
Stahel
Philip F
PF
D000818:Animals; D001522:Behavior, Animal / Q000502:physiology; D001812:Blood-Brain Barrier / Q000502:physiology; D001921:Brain / Q000473:pathology / Q000503:physiopathology; D002490:Central Nervous System / Q000276:immunology*; D003167:Complement Activation; D003165:Complement System Proteins / Q000276:immunology*; D016489:Head Injuries, Closed / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D018696:Neuroprotective Agents / Q000378:metabolism*; D011951:Receptors, Complement / Q000235:genetics / Q000378:metabolism*; D017463:Receptors, Complement 3b
C081470:Cr1l protein, mouse; D018696:Neuroprotective Agents; D011951:Receptors, Complement; D017463:Receptors, Complement 3b; D003165:Complement System Proteins