Blocking of bradykinin receptor B1 protects from focal closed head injury in mice by reducing axonal damage and astroglia activation

Christiane Albert-Weissenberger, Christian Stetter, Sven G. Meuth, Kerstin Goebel, Michael Bader, Anna-Leena Siren, Christoph Kleinschnitz*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

31 Citations (Web of Science)

Abstract

The two bradykinin receptors B1R and B2R are central components of the kallikrein-kinin system with different expression kinetics and binding characteristics. Activation of these receptors by kinins triggers inflammatory responses in the target organ and in most situations enhances tissue damage. We could recently show that blocking of B1R, but not B2R, protects from cortical cryolesion by reducing inflammation and edema formation. In the present study, we investigated the role of B1R and B2R in a closed head model of focal traumatic brain injury (TBI; weight drop). Increased expression of B1R in the injured hemispheres of wild-type mice was restricted to the later stages after brain trauma, i.e. day 7 (P0.05). Mice lacking the B1R, but not the B2R, showed less functional deficits on day 3 (P
Original languageEnglish
Pages (from-to)1747-1756
JournalJournal of Cerebral Blood Flow and Metabolism
Volume32
Issue number9
DOIs
Publication statusPublished - Sep 2012

Keywords

  • astrocytes
  • beta-APP
  • closed head injury
  • kinin receptors
  • R-715
  • TNF-alpha

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