INT169533
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Some recent studies have demonstrated that expression of gp91phox increases in brain after intracerebral hemorrhage, resulting in enhanced lipid peroxidation [24,41]. | |||||||||||||||
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Consistent with a direct effect of IL-6 on Nox2 expression, direct systemic injection of IL-6 into mice increased Nox2 protein and activity, confirming the ability of peripheral IL-6 to mediate increased Nox2 expression and superoxide production in brain. | |||||||||||||||
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Increased Nox2 protein expression in brain of aged animals is attenuated in IL-6-/- mice | |||||||||||||||
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IL-6-/- mice lack the age-related increase in Nox2 expression and superoxide production observed in old wild-type mice. | |||||||||||||||
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In the context of chronically elevated peripheral IL-6 in aged animals, on the other hand, we wished to determine whether aging was associated with an increase in Nox2 expression in brain, by analyzing Nox2 protein expression in young (4 month old) and old (24 month old) mouse brain. | |||||||||||||||
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The robust induction of Nox2 expression and activity we observed led us to ask whether PV inhibitory interneurons might also be selectively lost during aging, as well. | |||||||||||||||
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More importantly, direct application of IL-6 to cultured neurons resulted in a significant increase in Nox-2 expression and superoxide production which was fully blocked by the NF? | |||||||||||||||
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B signaling can directly induce Nox2 expression in neurons. | |||||||||||||||
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Moreover, we recently demonstrated that IL-6 can directly induce and activate Nox2 protein expression in cultured neurons[15], but in that study in young mice, acute peripheral injection of IL-6 failed to induce brain Nox2 expression. | |||||||||||||||
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To quantify the age-related increase in Nox2 expression, and assess whether IL-6 was involved in this process, we determined levels of Nox2 protein in young and old wild-type (C57BL/6) and IL-6-deficient (IL-6-/-) animals. | |||||||||||||||
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Gp91phox gene deletion reduces 3-NT generation after TBI in vivo | |||||||||||||||
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Gp91phox gene deletion reduces 3-NT generation after TBI in vivo | |||||||||||||||
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More importantly, direct application of IL-6 to cultured neurons resulted in a significant increase in Nox-2 expression and superoxide production which was fully blocked by the NF? | |||||||||||||||
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, 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.
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Protein levels of gp91phox were not increased after TBI in the contralateral hemisphere of Wt mice. | |||||||||||||||
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Gp91phox expression increased mainly in amoeboid-shaped microglial cells of the ipsilateral hemisphere of Wt mice after TBI. | |||||||||||||||
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Repeated intraperitoneal injection of IL-6 (5 µg/kg i.p. every 12 hours times 3) in mice significantly increased expression of Nox2 protein in brain (Fig. 2d, top) and resulted in substantially higher superoxide levels, as documented by DHE oxidation (Fig. 2d, bottom).
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Nox2 expression was induced in dorsal horn microglia immediately after L5 spinal nerve transection (SNT). | |||||||||||||||
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We then evaluated synaptosomes prepared from young and old IL-6-/- mice, and found that compared to old wild-type controls, IL-6-/- mice had an attenuation of age-induced increases in Nox2 O2 consumption (Fig. 3a, (F(1,6)? | |||||||||||||||
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In the central nervous system, Noh and Koh (2000) were able to demonstrate increased NADPH oxidase-derived (NOX2) ROS production in cortical cultures in response to zinc exposure [72]. | |||||||||||||||
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