Abstract
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.
Publication types
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
Animals
-
Behavior, Animal / physiology
-
Blood-Brain Barrier / physiology
-
Brain / pathology
-
Brain / physiopathology
-
Central Nervous System / immunology*
-
Complement Activation*
-
Complement System Proteins / immunology*
-
Head Injuries, Closed / immunology
-
Head Injuries, Closed / pathology
-
Head Injuries, Closed / physiopathology*
-
Mice
-
Mice, Inbred C57BL
-
Mice, Transgenic
-
Neuroprotective Agents / metabolism*
-
Receptors, Complement / genetics
-
Receptors, Complement / metabolism*
-
Receptors, Complement 3b
Substances
-
Cr1l protein, mouse
-
Neuroprotective Agents
-
Receptors, Complement
-
Receptors, Complement 3b
-
Complement System Proteins