ArticleJournal of neurochemistry2011
Cold pre-conditioning neuroprotection depends on TNF-α and is enhanced by blockade of interleukin-11.
Article in Journal of neurochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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
16 citing papers in PubMed, 74 citations in OpenAlex.
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- Insulin-like growth factor-1 abrogates microglial oxidative stress and TNF-α responses to spreading depression.Journal of neurochemistry · 2013Article
- Neuroprotective activity of peripherally administered liver growth factor in a rat model of Parkinson's disease.PloS one · 2013Article
- Therapeutic hypothermia as a neuroprotective strategy in neonatal hypoxic-ischemic brain injury and traumatic brain injury.Current molecular medicine · 2012Review
- Pregnant serum induces neuroinflammation and seizure activity via TNFα.Experimental neurology · 2012Article
- Cytokines reduce toxic effects of ethanol on oligodendroglia.Neurochemical research · 2011Article
- Modeling neural immune signaling of episodic and chronic migraine using spreading depression in vitro.Journal of visualized experiments : JoVE · 2011Article
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Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Cold pre-conditioning reduces subsequent brain injury in small animals but the underlying mechanisms remain undefined. As hypothermia triggers systemic macrophage tumor necrosis factor alpha (TNF-α) production and other neural pre-conditioning stimuli depend on this cytokine, we reasoned that microglia and TNF-α would be similarly involved with cold pre-conditioning neuroprotection. Also, as slice cultures closely approximate their in vivo counterpart and include quiescent microglia, we used rat hippocampal slice cultures to confirm this hypothesis. Furthermore, inflammatory cytokine gene screening with subsequent PCR and immunostaining confirmation of targeted mRNA and related protein changes showed that cold pre-conditioning triggered a significant rise in TNF-α that localized to microglia and a significant rise in interleukin (IL)-11 that localized mainly to hippocampal pyramidal neurons and, more rarely, astrocytes. Importantly, co-stimulation with cold and IL-11, an anti-inflammatory cytokine that inhibits TNF-α expression, abrogated the otherwise evident protection. Instead, cold pre-conditioning coupled with blockade of IL-11 signaling further enhanced neuroprotection from that seen with cold pre-conditioning alone. Thus, physiological activation of brain pro-inflammatory cytokine signaling, and its amplification by inhibition of coincident anti-inflammatory cytokine signaling, may be opportune targets for the development of novel therapeutics that can mimic the protection seen in cold pre-conditioning.
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Registered trials
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