ArticleThe Journal of biological chemistry2008
Tumor necrosis factor-alpha potentiates intraneuronal Ca2+ signaling via regulation of the inositol 1,4,5-trisphosphate receptor.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- Autocrine positive feedback of tumor necrosis factor from activated microglia proposed to be of widespread relevance in chronic neurological disease.Pharmacology research & perspectives · 2023Review
- Chronic cerebral aspects of long COVID, post-stroke syndromes and similar states share their pathogenesis and perispinal etanercept treatment logic.Pharmacology research & perspectives · 2022Review
- CREB regulates the expression of type 1 inositol 1,4,5-trisphosphate receptors.Journal of cell science · 2021Article
- Background to new treatments for COVID-19, including its chronicity, through altering elements of the cytokine storm.Reviews in medical virology · 2021Review
- Article
- Calcium Ions Aggravate Alzheimer's Disease Through the Aberrant Activation of Neuronal Networks, Leading to Synaptic and Cognitive Deficits.Frontiers in molecular neuroscience · 2021Review
- Negative Feedback Role of Astrocytes in Shaping Excitation in Brain Cell Co-cultures.Frontiers in cellular neuroscience · 2021Article
- Androgen Receptor-Mediated Regulation of Intracellular Calcium in Human Airway Smooth Muscle Cells.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2019Article
- The Inflammatory Nature of Post-surgical Delirium Predicts Benefit of Agents With Anti-TNF Effects, Such as Dexmedetomidine.Frontiers in neuroscience · 2018Article
- The meteorology of cytokine storms, and the clinical usefulness of this knowledge.Seminars in immunopathology · 2017Review
- Scutellarin as a Potential Therapeutic Agent for Microglia-Mediated Neuroinflammation in Cerebral Ischemia.Neuromolecular medicine · 2016Review
- Amyloid β: one of three danger-associated molecules that are secondary inducers of the proinflammatory cytokines that mediate Alzheimer's disease.British journal of pharmacology · 2015Review
- A Neurologist's Guide to TNF Biology and to the Principles behind the Therapeutic Removal of Excess TNF in Disease.Neural plasticity · 2015Review
- Tumor necrosis factor-alpha-induced reduction of glomerular filtration rate in rats with fulminant hepatic failure.Laboratory investigation; a journal of technical methods and pathology · 2014Article
- The role of pro-inflammatory S100A9 in Alzheimer's disease amyloid-neuroinflammatory cascade.Acta neuropathologica · 2014Article
- Calcium dysregulation and neuroinflammation: discrete and integrated mechanisms for age-related synaptic dysfunction.Ageing research reviews · 2013Review
- Early intervention with a small molecule inhibitor for tumor necrosis factor-α prevents cognitive deficits in a triple transgenic mouse model of Alzheimer's disease.Journal of neuroinflammation · 2012Article
- Tumor necrosis factor-alpha and the roles it plays in homeostatic and degenerative processes within the central nervous system.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2012Review
- Inhibition of soluble tumor necrosis factor ameliorates synaptic alterations and Ca2+ dysregulation in aged rats.PloS one · 2012Article
- The dual role of the neuroinflammatory response after ischemic stroke: modulatory effects of hypothermia.Journal of neuroinflammation · 2010Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Inflammatory events have long been implicated in initiating and/or propagating the pathophysiology associated with a number of neurological diseases. In addition, defects in Ca2+-handling processes, which shape membrane potential, influence gene transcription, and affect neuronal spiking patterns, have also been implicated in disease progression and cognitive decline. The mechanisms underlying the purported interplay that exists between neuroinflammation and Ca2+ homeostasis have yet to be defined. Herein, we describe a novel neuron-intrinsic pathway in which the expression of the type-1 inositol 1,4,5-trisphosphate receptor is regulated by the potent pro-inflammatory cytokine tumor necrosis factor-alpha. Exposure of primary murine neurons to tumor necrosis factor-alpha resulted in significant enhancement of Ca2+ signals downstream of muscarinic and purinergic stimulation. An increase in type-1 inositol 1,4,5-trisphosphate receptor mRNA and protein steady-state levels following cytokine exposure positively correlated with this alteration in Ca2+ homeostasis. Modulation of Ca2+ responses arising from this receptor subtype and its downstream effectors may exact significant consequences on neuronal function and could underlie the compromise in neuronal activity observed in the setting of chronic neuroinflammation, such as that associated with Parkinson disease and Alzheimer disease.
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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.