TY - CHAP
T1 - Microglial activation and intracerebral hemorrhage
AU - Gao, Z.
AU - Wang, Jian
AU - Thiex, R.
AU - Rogove, A. D.
AU - Heppner, F. L.
AU - Tsirka, S. E.
PY - 2008/1/1
Y1 - 2008/1/1
N2 - Microglia activate upon injury, migrate to the injury site, proliferate locally, undergo morphological and gene expression changes, and phagocytose injured and dying cells. Cytokines and proteases secreted by these cells contribute to the injury and edema formed. We studied the injury outcome after local elimination/paralysis of microglia. Adult male mice were subjected to intracerebral hemorrhage (ICH) by intra-caudate injection of either collagenase or autologous blood. Mice survived for different periods of time, and were subsequently evaluated for neurological deficits, size of the hematoma, and microglia activation. Mice expressing an fms-GFP transgene or the CD1 1b-HSVTK transgene were also used. For elimination of monocy-tes/macrophages, CD1 1b-HSVTK mice were treated with ganciclovir prior to hemorrhage. Modifiers of microglial activation were also used. Induction of ICH resulted in robust microglia activation and recruitment of macrophages. Inactivation of these cells, genetically or pharmacologically, pointed to a critical role of the time of such inactivation, indicating that their role is distinct at different time points following injury. Edema formation is decreased when microglia activation is inhibited, and neurological outcomes are improved. Microglia, as immunomodulatory cells, have the ability to modify the final presentation of ICH.
AB - Microglia activate upon injury, migrate to the injury site, proliferate locally, undergo morphological and gene expression changes, and phagocytose injured and dying cells. Cytokines and proteases secreted by these cells contribute to the injury and edema formed. We studied the injury outcome after local elimination/paralysis of microglia. Adult male mice were subjected to intracerebral hemorrhage (ICH) by intra-caudate injection of either collagenase or autologous blood. Mice survived for different periods of time, and were subsequently evaluated for neurological deficits, size of the hematoma, and microglia activation. Mice expressing an fms-GFP transgene or the CD1 1b-HSVTK transgene were also used. For elimination of monocy-tes/macrophages, CD1 1b-HSVTK mice were treated with ganciclovir prior to hemorrhage. Modifiers of microglial activation were also used. Induction of ICH resulted in robust microglia activation and recruitment of macrophages. Inactivation of these cells, genetically or pharmacologically, pointed to a critical role of the time of such inactivation, indicating that their role is distinct at different time points following injury. Edema formation is decreased when microglia activation is inhibited, and neurological outcomes are improved. Microglia, as immunomodulatory cells, have the ability to modify the final presentation of ICH.
KW - edema
KW - intracerebral hemorrhage
KW - Microglia
KW - tissue plasminogen activator
UR - http://www.scopus.com/inward/record.url?scp=85052608822&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85052608822&partnerID=8YFLogxK
U2 - 10.1007/978-3-211-09469-3_11
DO - 10.1007/978-3-211-09469-3_11
M3 - Chapter
C2 - 19066082
AN - SCOPUS:85052608822
SN - 9783211094686
T3 - Acta Neurochirurgica, Supplementum
SP - 51
EP - 53
BT - Cerebral Hemorrhage
PB - Springer-Verlag Wien
ER -