Epigenetic modulation of gene expression governs the brain's response to injury

Simon, Roger P.

doi:10.1016/j.neulet.2015.12.024

Cited by 15 publications

(6 citation statements)

References 54 publications

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“…SPRR1 may be induced by hypomethylating agents and its expression may be modulated by histone modification [ 97 ]. Similarly to the impact of 5-azacytidine on keratinocytes, SPRR1 expression is increased in these cells after treatment with an HDAC inhibitor such as sodium butyrate.…”

Section: Axon Growthmentioning

confidence: 99%

Brain Functional Reserve in the Context of Neuroplasticity after Stroke

et al. 2019

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Stroke is the second cause of death and more importantly first cause of disability in people over 40 years of age. Current therapeutic management of ischemic stroke does not provide fully satisfactory outcomes. Stroke management has significantly changed since the time when there were opened modern stroke units with early motor and speech rehabilitation in hospitals. In recent decades, researchers searched for biomarkers of ischemic stroke and neuroplasticity in order to determine effective diagnostics, prognostic assessment, and therapy. Complex background of events following ischemic episode hinders successful design of effective therapeutic strategies. So far, studies have proven that regeneration after stroke and recovery of lost functions may be assigned to neuronal plasticity understood as ability of brain to reorganize and rebuild as an effect of changed environmental conditions. As many neuronal processes influencing neuroplasticity depend on expression of particular genes and genetic diversity possibly influencing its effectiveness, knowledge on their mechanisms is necessary to understand this process. Epigenetic mechanisms occurring after stroke was briefly discussed in this paper including several mechanisms such as synaptic plasticity; neuro-, glio-, and angiogenesis processes; and growth of axon.

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Section: Axon Growthmentioning

confidence: 99%

Brain Functional Reserve in the Context of Neuroplasticity after Stroke

et al. 2019

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“…Alternatively, if a transcript’s expression was induced or suppressed as part of a compensatory and/or adaptive response to AHR, then its expression might also appear normalized by loss of ASIC1a, since ASIC1a −/− mice lack AHR ( 66 ). In the latter case, such transcripts might be beneficial and/or have protective effects ( 38 , 78 , 84 ). We also conceived that signature 1 transcripts might have no bearing or role in AHR.…”

Section: Resultsmentioning

confidence: 99%

“…This finding suggests that the majority of transcripts comprising signature 1 were likely compensatory and/or potentially protective in nature. Indeed, previous studies have demonstrated that a sublethal stressor in the nervous system can produce a “damage refractory” state that protects the nervous system from subsequent injury (preconditioning and tolerance) ( 38 , 78 , 84 ). In rats preconditioned with brief seizures, the transcriptional response of the hippocampus to a subsequent seizure is characterized by a neuroprotective suppression of Ca 2+ signaling ( 38 ).…”

Section: Discussionmentioning

confidence: 99%

The vagal ganglia transcriptome identifies candidate therapeutics for airway hyperreactivity

Reznikov

Meyerholz

Alaiwa

et al. 2018

American Journal of Physiology-Lung Cellular and Molecular Phys

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Mainstay therapeutics are ineffective in some people with asthma, suggesting a need for additional agents. In the current study, we used vagal ganglia transcriptome profiling and connectivity mapping to identify compounds beneficial for alleviating airway hyperreactivity (AHR). As a comparison, we also used previously published transcriptome data from sensitized mouse lungs and human asthmatic endobronchial biopsies. All transcriptomes revealed agents beneficial for mitigating AHR; however, only the vagal ganglia transcriptome identified agents used clinically to treat asthma (flunisolide, isoetarine). We also tested one compound identified by vagal ganglia transcriptome profiling that had not previously been linked to asthma and found that it had bronchodilator effects in both mouse and pig airways. These data suggest that transcriptome profiling of the vagal ganglia might be a novel strategy to identify potential asthma therapeutics.

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“…Nitrosative stress may lead to BBB breakdown, inflammation, and caspase activation, which ultimately lead to cell apoptosis through interacting with different cellular signaling pathways including matrix metalloproteinase, high-mobility group box 1, toll-like receptors 2 and 4, poly(ADP-ribose) polymerase, Src, Rhoassociated protein kinase (ROCK), and glycogen synthase kinase (GSK)-3β (Radi et al, 2015). Oxidative stress may also influence epigenetic mechanisms (i.e., DNA methylation, histone modification, microRNAs) (Zhao et al, 2016;Narne et al, 2017), well known to be implicated in neuroprotection (Felling and Song, 2015;Simon, 2016;Chandran et al, 2017). Therefore, it has been suggested that ROS may contribute themselves to neuronal recovery after ischemic stroke.…”

Section: Hausenloy Et Al 2014mentioning

confidence: 99%

Neutrophil-Related Oxidants Drive Heart and Brain Remodeling After Ischemia/Reperfusion Injury

2020

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The inflammatory response associated with myocardial and brain ischemia/reperfusion injury (IRI) is a critical determinant of tissue necrosis, functional organ recovery, and long-term clinical outcomes. In the post-ischemic period, reactive oxygen species (ROS) are involved in tissue repair through the clearance of dead cells and cellular debris. Neutrophils play a critical role in redox signaling due to their early recruitment and the large variety of released ROS. Noteworthy, ROS generated during IRI have a relevant role in both myocardial healing and activation of neuroprotective pathways. Anatomical and functional differences contribute to the responses in the myocardial and brain tissue despite a significant gene overlap. The exaggerated activation of this signaling system can result in adverse consequences, such as cell apoptosis and extracellular matrix degradation. In light of that, blocking the ROS cascade might have a therapeutic implication for cardiomyocyte and neuronal loss after acute ischemic events. The translation of these findings from preclinical models to clinical trials has so far failed because of differences between humans and animals, difficulty of agents to penetrate into specific cellular organs, and specifically unravel oxidant and antioxidant pathways. Here, we update knowledge on ROS cascade in IRI, focusing on the role of neutrophils. We discuss evidence of ROS blockade as a therapeutic approach for myocardial infarction and ischemic stroke.

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Epigenetic modulation of gene expression governs the brain's response to injury

Cited by 15 publications

References 54 publications

Brain Functional Reserve in the Context of Neuroplasticity after Stroke

Brain Functional Reserve in the Context of Neuroplasticity after Stroke

The vagal ganglia transcriptome identifies candidate therapeutics for airway hyperreactivity

Neutrophil-Related Oxidants Drive Heart and Brain Remodeling After Ischemia/Reperfusion Injury

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