ArticleMolecular and cellular neurosciences2009
Proinflammatory cytokines provoke oxidative damage to actin in neuronal cells mediated by Rac1 and NADPH oxidase.
Article in Molecular and cellular neurosciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 60 citations in OpenAlex.
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- Alaska's Flora as a Treatment for Cancer.International journal of biopharmaceutical sciences · 2024Article
- Quercetin suppresses ROS production and migration by specifically targeting Rac1 activation in gliomas.Frontiers in pharmacology · 2024Article
- Chemokine Receptor Antagonists Prevent and Reverse Cofilin-Actin Rod Pathology and Protect Synapses in Cultured Rodent and Human iPSC-Derived Neurons.Biomedicines · 2024Article
- Characterization of a Human Neuronal Culture System for the Study of Cofilin-Actin Rod Pathology.Biomedicines · 2023Article
- Sphingolipids as Regulators of Neuro-Inflammation and NADPH Oxidase 2.Neuromolecular medicine · 2021Review
- Importance of the commissural nucleus of the solitary tract in renovascular hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Article
- Ligand-activated PPARδ inhibits angiotensin II-stimulated hypertrophy of vascular smooth muscle cells by targeting ROS.PloS one · 2019Article
- TNF-α Increases Production of Reactive Oxygen Species through Cdk5 Activation in Nociceptive Neurons.Frontiers in physiology · 2018Article
- The proinflammatory cytokine tumor necrosis factor-α excites subfornical organ neurons.Journal of neurophysiology · 2017Article
- Actin filaments-A target for redox regulation.Cytoskeleton (Hoboken, N.J.) · 2016Review
- Redox Control of Multidrug Resistance and Its Possible Modulation by Antioxidants.Oxidative medicine and cellular longevity · 2016Review
- Reperfusion injury and reactive oxygen species: The evolution of a concept.Redox biology · 2015Review
- Determination of protein carbonyls in plasma, cell extracts, tissue homogenates, isolated proteins: Focus on sample preparation and derivatization conditions.Redox biology · 2015Review
- Homocysteine disrupts outgrowth of microvascular endothelium by an iNOS-dependent mechanism.Microcirculation (New York, N.Y. : 1994) · 2014Article
- Article
- Oxygen radicals elicit paralysis and collapse of spinal cord neuron growth cones upon exposure to proinflammatory cytokines.BioMed research international · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The proinflammatory cytokines TNFalpha and Il-1beta orchestrate the progression of CNS inflammation, which substantially contributes to neurodegeneration in many CNS pathologies. TNFalpha and Il-1beta stimulate actin filament reorganization in non-neuronal cells often accompanied by the formation of reactive oxygen species (ROS). Actin filament dynamics is vital for cellular plasticity, mitochondrial function, and gene expression despite being highly susceptible to oxidative damage. We demonstrated that, in neuronal cells, TNFalpha and Il-1beta stimulate a transient, redox-dependent reorganization of the actin cytoskeleton into lamellipodia under the regulation of Rac1 and a neuronal NADPH oxidase as the source of ROS. The persistent presence of intracellular ROS provoked oxidative damage (carbonylation) to actin coinciding with the loss of lamellipodia and arrest of cellular plasticity. Inhibition of NADPH oxidase activity or Rac1 abolished the adverse effects of cytokines. These findings suggest that oxidative damage to the neuronal actin cytoskeleton could represent a key step in CNS neurodegeneration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.