Microglial activation and intracerebral hemorrhage

Z. Gao, Jian Wang, R. Thiex, A. D. Rogove, F. L. Heppner, S. E. Tsirka

Research output: Chapter in Book/Report/Conference proceedingChapter

32 Scopus citations


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.

Original languageEnglish (US)
Title of host publicationCerebral Hemorrhage
PublisherSpringer-Verlag Wien
Number of pages3
ISBN (Print)9783211094686
StatePublished - Jan 1 2008
Externally publishedYes

Publication series

NameActa Neurochirurgica, Supplementum
ISSN (Print)0065-1419


  • edema
  • intracerebral hemorrhage
  • Microglia
  • tissue plasminogen activator

ASJC Scopus subject areas

  • Surgery
  • Clinical Neurology


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