Immunohistochemical study of p47Phox and gp91Phox distributions in rat brain

Kim, Myeung Ju; Shin, Kyung Sue; Chung, Young Bae; Jung, Kee Wook; Ik, Choong; Shin, Dong Hoon

doi:10.1016/j.brainres.2005.01.066

Cited by 65 publications

(34 citation statements)

References 16 publications

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“…In vitro studies have shown NOX expression in neurons, astrocytes, and in microglia [222]. Immunohistochemical studies have shown that NOX subunits are widely distributed in the cortex, the hippocampus, and in the cerebellum in vivo [227] [228] [229] [230]. NOX has been documented to increase in the brain after experimental stroke [231] and we have shown that NOX derived from circulating cells contributes significantly to stroke pathogenesis compare to the brain resident cells [232].…”

Section: Reactive Oxygen Speciesmentioning

confidence: 99%

Innate Inflammatory Responses in Stroke: Mechanisms and Potential Therapeutic Targets

Kim¹,

Kawabori²,

Yenari³

2014

CMC

220

191

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Stroke is a frequent cause of long-term disability and death worldwide. Ischemic stroke is more commonly encountered compared to hemorrhagic stroke, and leads to tissue death by ischemia due to occlusion of a cerebral artery. Inflammation is known to result as a result of ischemic injury, long thought to be involved in initiating the recovery and repair process. However, work over the past few decades indicates that aspects of this inflammatory response may in fact be detrimental to stroke outcome. Acutely, inflammation appears to have a detrimental effect, and anti-inflammatory treatments have been been studied as a potential therapeutic target. Chronically, reports suggest that post-ischemic inflammation is also essential for the tissue repairing and remodeling. The majority of the work in this area has centered around innate immune mechanisms, which will be the focus of this review. This review describes the different key players in neuroinflammation and their possible detrimental and protective effects in stroke. A better understanding of the roles of the different immune cells and their temporal profile of damage versus repair will help to clarify more effective modulation of inflammation post stroke. Introduction Stroke refers to conditions caused by occlusion and/or rupture of blood vessels in the brain, and is a leading cause of death and disability in the industrialized world.

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Section: Reactive Oxygen Speciesmentioning

confidence: 99%

Innate Inflammatory Responses in Stroke: Mechanisms and Potential Therapeutic Targets

Kim¹,

Kawabori²,

Yenari³

2014

CMC

220

191

View full text Add to dashboard Cite

show abstract

“…During oxidation, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-derived reactive oxygen species (ROS) play crucial roles in BBB breakdown and brain edema2324. The main NADPH oxidase subunit expressed in brain tissue is gp91 phox 25. It maintains enzyme function by producing oxygen radicals.…”

mentioning

confidence: 99%

Rhein and rhubarb similarly protect the blood-brain barrier after experimental traumatic brain injury via gp91phox subunit of NADPH oxidase/ROS/ERK/MMP-9 signaling pathway

Wang

Fan

Tang

et al. 2016

Sci Rep

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Oxidative stress chiefly contributes to the disruption of the BBB following traumatic brain injury (TBI). The Chinese herbal medicine rhubarb is a promising antioxidant in treating TBI. Here we performed in vivo and in vitro experiments to determine whether rhubarb and its absorbed bioactive compound protected the BBB after TBI by increasing ZO-1 expression through inhibition of gp91phox subunit of NADPH oxidase/ROS/ERK/MMP-9 pathway. Rats were subjected to the controlled cortical impact (CCI) model, and primary rat cortical astrocytes were exposed to scratch-wound model. The liquid chromatography with tandem mass spectrometry method showed that rhein was the compound absorbed in the brains of CCI rats after rhubarb administration. The wet-dry weights and Evans blue measurements revealed that rhubarb and rhein ameliorated BBB damage and brain edema in CCI rats. Western blots showed that rhubarb and rhein downregulated GFAP in vitro. RT-PCR, immunohistochemistry, Western blot and dichlorodihydrofluorescein diacetate analysis indicated that rhubarb prevented activation of gp91phox subunit of NADPH oxidase induced ROS production, subsequently inhibited ERK/MMP-9 pathway in vivo and in vitro. Interestingly, rhein and rhubarb similarly protected the BBB by inhibiting this signaling cascade. The results provide a novel herbal medicine to protect BBB following TBI via an antioxidative molecular mechanism.

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“…GH, IGF-1 and growth factors generate ROS via NAD(P)H oxidases (NOX) (Rollo 2002(Rollo , 2006(Rollo , 2007a. NOX are expressed in microglia, astrocytes, neurons and cerebrovasculature but especially in striatum and hippocampus (Noh and Koh 2000;Serrano et al 2003;Kim et al 2005;Tejada-Simon et al 2005). ROS signalling is essential for long-term potentiation (Kamsler and Segal 2003;Tejada-Simon et al 2005).…”

Section: Oxidative Stress Hypothesismentioning

confidence: 99%

Modifier Selection by Transgenes: The Case of Growth Hormone Transgenesis and Hyperactive Circling Mice

et al. 2008

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Deleterious impacts of major mutations can be ameliorated by stabilising selection acting on modifier genes. We hypothesise that a new hyperactive circling mouse (counterspin: Cr) arises when modifier genes inadvertently selected to ameliorate the negative impacts of a growth hormone transgenic insertion segregate into the normal genetic background that lacks the transgene. We hypothesise that such modifiers generate a phenotype ''mirror image'' to the transgenics on the otherwise normal background. We highlight this by testing a priori hypotheses that counterspin and transgenic growth hormone mice deviate oppositely from normal mice across a broad spectrum of characteristics. Results spanning growth, sensorimotor performance, cognition and striatal neurotransmitters provide strong circumstantial evidence for the hypothesis. In a more direct test for selection in the transgenic mice, we found that those examined in 2008 slept *3 h/d less than they did 14 years ago (P \ 0.0005). This is a profound change strongly supporting the reality of modifier selection in these mice. Our results highlight that modifiers may act powerfully on genetically engineered constructs given a genetically variable background. Furthermore, we suggest that modifier selection might provide a novel method for deriving genetic models, and specifically, models phenotypically opposite to engineered constructs or natural mutations.

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Immunohistochemical study of p47Phox and gp91Phox distributions in rat brain

Cited by 65 publications

References 16 publications

Innate Inflammatory Responses in Stroke: Mechanisms and Potential Therapeutic Targets

Innate Inflammatory Responses in Stroke: Mechanisms and Potential Therapeutic Targets

Rhein and rhubarb similarly protect the blood-brain barrier after experimental traumatic brain injury via gp91phox subunit of NADPH oxidase/ROS/ERK/MMP-9 signaling pathway

Modifier Selection by Transgenes: The Case of Growth Hormone Transgenesis and Hyperactive Circling Mice

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