The absence of the CD163 receptor has distinct temporal influences on intracerebral hemorrhage outcomes
| Autor: | Jenna L Leclerc, Andrew S Lampert, Søren K. Moestrup, Terrie Vasilopoulos, Pia Svendsen, Claudia Loyola Amador, Brandon Schlakman, Sylvain Doré |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
Male
Receptors Cell Surface/genetics 0301 basic medicine Pathology Hematoma/genetics Hemoglobins Mice iron 0302 clinical medicine Neovascularization Pathologic/genetics oxidative stress Gliosis Receptor Mice Knockout Hematoma Neovascularization Pathologic Microglia Brain Antigens CD/genetics heme oxygenase stroke medicine.anatomical_structure Neurology Cerebral Hemorrhage/genetics Blood-Brain Barrier medicine.symptom Cardiology and Cardiovascular Medicine Gliosis/etiology medicine.medical_specialty Iron Antigens Differentiation Myelomonocytic Receptors Cell Surface Brain damage Blood–brain barrier 03 medical and health sciences Antigens CD medicine Animals Brain/pathology Scavenger receptor Cerebral Hemorrhage Intracerebral hemorrhage business.industry Hemoglobins/metabolism Antigens Differentiation Myelomonocytic/genetics Recovery of Function medicine.disease Mice Inbred C57BL 030104 developmental biology Neurology (clinical) business Iron/metabolism CD163 Neuroscience Psychomotor Performance 030217 neurology & neurosurgery |
| Zdroj: | Leclerc, J L, Lampert, A S, Loyola Amador, C, Schlakman, B, Vasilopoulos, T, Svendsen, P, Moestrup, S K & Doré, S 2018, ' The absence of the CD163 receptor has distinct temporal influences on intracerebral hemorrhage outcomes ', Journal of Cerebral Blood Flow and Metabolism, vol. 38, no. 2, pp. 262-273 . https://doi.org/10.1177/0271678X17701459 |
| ISSN: | 1559-7016 0271-678X |
| Popis: | Hemoglobin (Hb) toxicity precipitates secondary brain damage following intracerebral hemorrhage (ICH). CD163 is an anti-inflammatory Hb scavenger receptor and CD163-positive macrophages/microglia locally accumulate post-bleed, yet no studies have investigated the role of CD163 after ICH. ICH was induced in wildtype and CD163−/− mice and various anatomical and functional outcomes were assessed. At 3 d, CD163−/− mice have 43.4 ± 5.0% (p = 0.0002) and 34.8 ± 3.4% (p = 0.0003) less hematoma volume and tissue injury, respectively. Whereas, at 10 d, CD163−/− mice have 49.2 ± 15.0% larger lesions (p = 0.0385). An inflection point was identified, where CD163−/− mice perform better on neurobehavioral testing and have less mortality before 4 d, but increased mortality and worse function after 4 d (p = 0.0389). At 3 d, CD163−/− mice have less Hb, iron, and blood–brain barrier dysfunction, increased astrogliosis and neovascularization, and no change in heme oxygenase 1 (HO1) expression. At 10 d, CD163−/− mice have increased iron and VEGF immunoreactivity, but no significant change in HO1 or astrogliosis. These novel findings reveal that CD163 deficiency has distinct temporal influences following ICH, with early beneficial properties but delayed injurious effects. While it is unclear why CD163 deficiency is initially beneficial, the late injurious effects are consistent with the key anti-inflammatory role of CD163 in the recovery phase of tissue damage. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|