Induction of heme oxygenase-1 after hyperosmotic opening of the blood- brain barrier

Jeremy D. Richmon, Kazumasa Fukuda, Nino Maida, Motoki Sato, Marcelle Bergeron, Frank R. Sharp, S. Scott Panter, L. J. Noble

Research output: Contribution to journalArticlepeer-review

49 Scopus citations


The induction of the stress protein heme oxygenase-1 (HO-1) was studied in the rat brain after intracarotid administration of hyperosmolar mannitol. HO-1 was immunolocalized in fixed sections of brain 24 h to 7 days after injection. Immunoglobulin G (IgG) was immunolocalized in adjacent sections to demonstrate areas of breakdown of the blood-brain barrier. Induction of HO-1 was also evaluated by Western immunoblots, performed at 24 h after the insult. Immunofluorescent double labelling with monoclonal antibodies to HO- 1 and either glial fibrillary acidic protein or the complement C3bi receptor was used to determine if glia/macrophages expressed HO-1. There was pronounced, widespread induction of HO-1 in the ipsilateral hemisphere and cerebellum by 24 h both by immunocytochemistry and by Western blots. This induction was markedly attenuated at later times. HO-1 was induced in astrocytes and microglia/macrophages in the ipsilateral hemisphere. In addition, the protein was induced in Bergmann glia and scattered microglia/macrophages in the cerebellum. The mechanism of induction of HO-1 in glia after opening of the blood-brain barrier could include exposure to heme proteins, denatured proteins and other plasma constituents known to induce HO-1. This glial induction may reflect a protective response of these cells.

Original languageEnglish (US)
Pages (from-to)108-118
Number of pages11
JournalBrain research
Issue number1
StatePublished - Jan 5 1998
Externally publishedYes


  • Astrocyte
  • Bergmann glia
  • Heat shock protein
  • Macrophage
  • Mannitol
  • Microglia

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology


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