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   Gp91phox (NOX2) in classically activated microglia exacerbates traumatic brain injury  
   
نویسنده dohi k. ,ohtaki h. ,nakamachi t. ,yofu s. ,satoh k. ,miyamoto k. ,song d. ,tsunawaki s. ,shioda s. ,aruga t.
منبع journal of neuroinflammation - 2010 - دوره : 7 - شماره : 0
چکیده    Background: we hypothesized that gp91phox(nox2),a subunit of nadph oxidase,generates superoxide anion (o2 -) and has a major causative role in traumatic brain injury (tbi). to evaluate the functional role of gp91phoxand reactive oxygen species (ros) on tbi,we carried out controlled cortical impact in gp91phoxknockout mice (gp91phox-/-). we also used a microglial cell line to determine the activated cell phenotype that contributes to gp91phoxgeneration.methods: unilateral tbi was induced in gp91phox-/-and wild-type (wt) mice (c57/b6j) (25-30 g). the expression and roles of gp91phoxafter tbi were investigated using immunoblotting and staining techniques. levels of o2 -and peroxynitrite were determined in situ in the mouse brain. the activated phenotype in microglia that expressed gp91phoxwas determined in a microglial cell line,bv-2,in the presence of ifnγ or il-4.results: gp91phoxexpression increased mainly in amoeboid-shaped microglial cells of the ipsilateral hemisphere of wt mice after tbi. the contusion area,number of tunel-positive cells,and amount of o2 -and peroxynitrite metabolites produced were less in gp91phox-/-mice than in wt. in the presence of ifnγ,bv-2 cells had increased inducible nitric oxide synthase and nitric oxide levels,consistent with a classical activated phenotype,and drastically increased expression of gp91phox.conclusions: classical activated microglia promote ros formation through gp91phoxand have an important role in brain damage following tbi. modulating gp91phoxand gp91phox-derived ros may provide a new therapeutic strategy in combating post-traumatic brain injury. © 2010 dohi et al; licensee biomed central ltd.
آدرس department of emergency and critical care medicine,showa university school of medicine,shinagawa-ku,tokyo 142-8555, Japan, department of anatomy,showa university school of medicine,shinagawa-ku,tokyo 142-8555, Japan, department of anatomy,showa university school of medicine,shinagawa-ku,tokyo 142-8555, Japan, department of anatomy,showa university school of medicine,shinagawa-ku,tokyo 142-8555, Japan, department of anatomy,showa university school of medicine,shinagawa-ku,tokyo 142-8555, Japan, department of emergency and critical care medicine,showa university school of medicine,shinagawa-ku,tokyo 142-8555, Japan, department of anatomy,showa university school of medicine,shinagawa-ku,tokyo 142-8555, Japan, department of infectious diseases,national research institute for child health and development,setagaya-ku,tokyo,157-8535, Japan, department of anatomy,showa university school of medicine,shinagawa-ku,tokyo 142-8555, Japan, department of emergency and critical care medicine,showa university school of medicine,shinagawa-ku,tokyo 142-8555, Japan
 
     
   
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