Deletion of the hemopexin or heme oxygenase-2 gene aggravates brain injury following stroma-free hemoglobin-induced intracerebral hemorrhage
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  • 作者:Bo Ma ; Jason Patrick Day ; Harrison Phillips ; Bryan Slootsky…
  • 关键词:Fluoro ; Jade ; Hemorrhagic stroke ; Iron ; Microglia ; Perls ; Phagocytosis
  • 刊名:Journal of Neuroinflammation
  • 出版年:2016
  • 出版时间:December 2016
  • 年:2016
  • 卷:13
  • 期:1
  • 全文大小:2,219 KB
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  • 作者单位:Bo Ma (1)
    Jason Patrick Day (1)
    Harrison Phillips (1)
    Bryan Slootsky (1)
    Emanuela Tolosano (2)
    Sylvain Doré (1) (3)

    1. Department of Anesthesiology, Center for Translational Research in Neurodegenerative Disease, University of Florida College of Medicine, P.O. Box 100159, Gainesville, FL, 32610, USA
    2. Departments of Molecular Biotechnology and Health Sciences, University of Torino, Torino, Italy
    3. Departments of Neuroscience, Neurology, Psychiatry, Psychology and Pharmaceutics, University of Florida College of Medicine, Gainesville, FL, 32610, USA
  • 刊物主题:Neurosciences; Neurology; Neurobiology; Immunology;
  • 出版者:BioMed Central
  • ISSN:1742-2094
文摘
Background Following intracerebral hemorrhage (ICH), red blood cells release massive amounts of toxic heme that causes local brain injury. Hemopexin (Hpx) has the highest binding affinity to heme and participates in its transport, while heme oxygenase 2 (HO2) is the rate-limiting enzyme for the degradation of heme. Microglia are the resident macrophages in the brain; however, the significance and role of HO2 and Hpx on microglial clearance of the toxic heme (iron-protoporphyrin IX) after ICH still remain understudied. Accordingly, we postulated that global deletion of constitutive HO2 or Hpx would lead to worsening of ICH outcomes.

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