Apolipoprotein E and apolipoprotein D expression in a murine model of singlet oxygen-induced cerebral stroke.
Apolipoprotein E (apoE)-deficient mice exhibit neuronal abnormalities similar to those in Alzheimer's disease and enhanced sensitivity to stroke-associated injuries. Here, we show that apoE deficiency results in impaired microglia/macrophage recruitment and accumulation after cerebral infarct. Astrogliosis and apolipoprotein D (apoD) expression are unaffected, suggesting that the neurological abnormalities of apoE-deficient mice could be due to impaired microglia/macrophage recruitment/accumulation, which is important for the clearance of neurodegenerative products via reverse cholesterol transport. To our knowledge, the results presented herein provide the first experimental evidence that brain microglia/macrophage recruitment/accumulation is affected by apoE deficiency. The insights gained from this study should facilitate the elucidation of the role of apoE in neurological disorders such as dementia with stroke and Alzheimer's disease.
Trieu
V N
VN
Department of Cardiovascular Biology, Department of Molecular Epidemiology, Parker Hughes Institute, 2665 Long Lake Road, St. Paul, Minnesota 55113, USA.
Uckun
F M
FM
D000544:Alzheimer Disease / Q000209:etiology; D000818:Animals; D001053:Apolipoproteins / Q000378:metabolism*; D053399:Apolipoproteins D; D001057:Apolipoproteins E / Q000172:deficiency* / Q000378:metabolism*; D004195:Disease Models, Animal; D006801:Humans; D007150:Immunohistochemistry; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D017628:Microglia / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D010100:Oxygen / Q000633:toxicity*; D026082:Singlet Oxygen; D020521:Stroke / Q000139:chemically induced* / Q000378:metabolism* / Q000473:pathology
D001053:Apolipoproteins; D053399:Apolipoproteins D; D001057:Apolipoproteins E; D026082:Singlet Oxygen; D010100:Oxygen