Mechanosensitive Regulation of Cortactin by p47
            <sup>phox</sup>

Montezano, Augusto C; Touyz, Rhian M.

doi:10.1161/circresaha.113.301495

Cited by 5 publications

(1 citation statement)

References 30 publications

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“…An alternative explanation is that NoxO1 has other functions than activating ROS production. For p47phox such functions have been reported [ 59 , 60 ]. Given the great similarity of NoxO1 to p47phox, an adapter function of NoxO1 beyond the one for Nox1-NoxA1 should not be dismissed.…”

Section: Discussionmentioning

confidence: 98%

Deletion of NoxO1 limits atherosclerosis development in female mice

et al. 2020

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Objective Oxidative stress is a risk factor for atherosclerosis. NADPH oxidases of the Nox family produce ROS but their contribution to atherosclerosis development is less clear. Nox2 promotes and Nox4 rather limits atherosclerosis. Although Nox1 with its cytosolic co-factors are largely expressed in epithelial cells, a role for Nox1 for atherosclerosis development was suggested. To further define the role of this homologue, the role of its essential cytosolic cofactor, NoxO1, was determined for atherosclerosis development with the aid of knockout mice. Methods and results Wildtype (WT) and NoxO1 knockout mice were treated with high fat diet and adeno-associated virus (AAV) overexpressing pro-protein convertase subtilisin/kexin type 9 (PCSK9) to induce hepatic low-density lipoprotein (LDL) receptor loss. As a result, massive hypercholesterolemia was induced and spontaneous atherosclerosis developed within three month. Deletion of NoxO1 reduced atherosclerosis formation in brachiocephalic artery and aortic arch in female but not male NoxO1−/− mice as compared to WT littermates. This was associated with a reduced pro-inflammatory cytokine signature in the plasma of female but not male NoxO1−/− mice. MACE-RNAseq of the vessel did not reveal this signature and the expression of the Nox1/NoxO1 system was low to not detectable. Conclusions The scaffolding protein NoxO1 plays some role in atherosclerosis development in female mice probably by attenuating the global inflammatory burden.

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Section: Discussionmentioning

confidence: 98%

Deletion of NoxO1 limits atherosclerosis development in female mice

et al. 2020

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RhoA/ROCK downregulates FPR2-mediated NADPH oxidase activation in mouse bone marrow granulocytes

Filina

Gabdoulkhakova

Safronova

2014

Cellular Signalling

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Carbon Nanotube Degradation in Macrophages: Live Nanoscale Monitoring and Understanding of Biological Pathway

et al. 2015

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Despite numerous applications, the cellular-clearance mechanism of multiwalled carbon nanotubes (MWCNTs) has not been clearly established yet. Previous in vitro studies showed the ability of oxidative enzymes to induce nanotube degradation. Interestingly, these enzymes have the common capacity to produce reactive oxygen species (ROS). Here, we combined material and life science approaches for revealing an intracellular way taken by macrophages to degrade carbon nanotubes. We report the in situ monitoring of ROS-mediated MWCNT degradation by liquid-cell transmission electron microscopy. Two degradation mechanisms induced by hydroxyl radicals were extracted from these unseen dynamic nanoscale investigations: a non-site-specific thinning process of the walls and a site-specific transversal drilling process on pre-existing defects of nanotubes. Remarkably, similar ROS-induced structural injuries were observed on MWCNTs after aging into macrophages from 1 to 7 days. Beside unraveling oxidative transformations of MWCNT structure, we elucidated an important, albeit not exclusive, biological pathway for MWCNT degradation in macrophages, involving NOX2 complex activation, superoxide production, and hydroxyl radical attack, which highlights the critical role of oxidative stress in cellular processing of MWCNTs.

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Mechanosensitive Regulation of Cortactin by p47 ^phox

Cited by 5 publications

References 30 publications

Deletion of NoxO1 limits atherosclerosis development in female mice

Deletion of NoxO1 limits atherosclerosis development in female mice

RhoA/ROCK downregulates FPR2-mediated NADPH oxidase activation in mouse bone marrow granulocytes

Carbon Nanotube Degradation in Macrophages: Live Nanoscale Monitoring and Understanding of Biological Pathway

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Mechanosensitive Regulation of Cortactin by p47 phox

Cited by 5 publications

References 30 publications

Deletion of NoxO1 limits atherosclerosis development in female mice

Deletion of NoxO1 limits atherosclerosis development in female mice

RhoA/ROCK downregulates FPR2-mediated NADPH oxidase activation in mouse bone marrow granulocytes

Carbon Nanotube Degradation in Macrophages: Live Nanoscale Monitoring and Understanding of Biological Pathway

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Mechanosensitive Regulation of Cortactin by p47 ^phox