Late preconditioning with isoflurane in cultured rat cortical neurones

Kaneko, Takaho; Yokoyama, Kazunori; Makita, Koshi

doi:10.1093/bja/aei228

Cited by 33 publications

(24 citation statements)

References 23 publications

(23 reference statements)

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“…In recent years, several studies showed that preconditioning by anesthetics exerted neuroprotective effects against cerebral ischemia in vitro and in vivo (Kawaguchi et al 2004, Kaneko et al 2005. As one of the important inhalational anesthetics, sevoflurane has been investigated in various models using both immediate and delayed preconditioning paradigms .…”

Section: Discussionmentioning

confidence: 99%

Identification of miRNAs Involved in the Protective Effect of Sevoflurane Preconditioning Against Hypoxic Injury in PC12 Cells

Sun

Liu

et al. 2015

Cell Mol Neurobiol

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The mechanism of sevoflurane preconditioning-induced neuroprotection is poorly understood. This study was aimed at identifying microRNAs (miRNAs) involved in the protective effect of sevoflurane preconditioning against hypoxic injury using the miRCURYTM LNA Array. The screened differentially expressed miRNAs were further validated using qRT-PCR. Finally, after transfection of miRNA (miR-101a or miR-34b) mimics or inhibitor, MTT and flow cytometry assays were used to evaluate cell survival and apoptosis in sevoflurane preconditioning. qRT-PCR confirmed the changes in expression of differentially expressed miRNAs that were screened by the microarray: down-regulation of rno-miR-101a, rno-miR-106b, and rno-miR-294 and up-regulation of rno-miR-883, rno-miR-16, and rno-miR-34b. MiR-101a and miR-34b were the most differentially expressed miRNAs. Sevoflurane preconditioning-inhibited apoptosis and preconditioning-enhanced cell viability of PC12 cells were significantly attenuated by transfection of miR-101a mimetic or miR-34b inhibitors, but were significantly enhanced by transfection of miR-34b mimetic. Therefore, a number of miRNAs, including miR-101a and miR-34b, might play important roles in the neuroprotection induced by sevoflurane preconditioning. Such miRNAs might provide novel targets for preventive and therapeutic strategies against cerebral ischemia-reperfusion injury.

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Section: Discussionmentioning

confidence: 99%

Identification of miRNAs Involved in the Protective Effect of Sevoflurane Preconditioning Against Hypoxic Injury in PC12 Cells

Sun

Liu

et al. 2015

Cell Mol Neurobiol

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“…For example, the protective preconditioning effect of volatile anesthetics has been demonstrated in neurons 11–15 , cardiac cells 32, 33 , epithelial cells 34 , and kidney cells 35 . Until now, however, no reports had considered innate cell sex in the response to anesthetics despite the sex differences reported in isoflurane preconditioning in vivo 1, 4, 5 .…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, most reports investigating anesthetic preconditioning at the cellular level in the brain have been limited to mixed-sex primary neuronal cultures 11–15 , leaving the role of astrocytes unexplored. Astrocytes comprise the majority of brain cells in mammals and are crucial in central nervous system function 16, 17 .…”

Section: Introductionmentioning

confidence: 99%

The Effect of Specialist Neurosciences Care on Outcome in Adult Severe Head Injury

Fuller

Bouamra²,

Woodford³

et al. 2011

Journal of Neurosurgical Anesthesiology

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Isoflurane exposure can protect the mammalian brain from subsequent insults like ischemic stroke. However, this protective preconditioning effect is sexually dimorphic, with isoflurane preconditioning decreasing male while exacerbating female brain damage in a mouse model of cerebral ischemia. Emerging evidence suggests that innate cell sex is an important factor in cell death, with brain cells having sex-specific sensitivities to different insults. We used an in vitro model of isoflurane preconditioning and ischemia to test the hypothesis that isoflurane preconditioning protects male astrocytes while having no effect or even a deleterious effect in female astrocytes following subsequent oxygen and glucose deprivation (OGD). Sex-segregated astrocyte cultures derived from postnatal day 0 to 1 mice were allowed to reach confluency before being exposed to either 0% (sham preconditioning) or 3% isoflurane preconditioning for 2 hours. Cultures were then returned to normal growth conditions for 22 hours before undergoing 10 hours of OGD. Twenty-four hours following OGD, cell viability was quantified using a lactate dehydrogenase assay. Isoflurane preconditioning increased cell survival following OGD compared to sham preconditioning independent of innate cell sex. More studies are needed to determine how cell type and cell sex may impact on anesthetic preconditioning and subsequent ischemic outcomes in the brain.

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“…Rapid and delayed preconditioning in both the heart and brain acts via different mechanisms. Generally, early preconditioning is related to a rapid response such as changes in ion channel permeability and post-translational modifications of proteins, while late preconditioning involves gene activation and protein synthesis [172,173,174,175]. …”

Section: Ncrnas In Brain Development and Ischemic Injurymentioning

confidence: 99%

Non-Coding RNAs as Potential Neuroprotectants against Ischemic Brain Injury

et al. 2013

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Over the past decade, scientific discoveries have highlighted new roles for a unique class of non-coding RNAs. Transcribed from the genome, these non-coding RNAs have been implicated in determining the biological complexity seen in mammals by acting as transcriptional and translational regulators. Non-coding RNAs, which can be sub-classified into long non-coding RNAs, microRNAs, PIWI-interacting RNAs and several others, are widely expressed in the nervous system with roles in neurogenesis, development and maintenance of the neuronal phenotype. Perturbations of these non-coding transcripts have been observed in ischemic preconditioning as well as ischemic brain injury with characterization of the mechanisms by which they confer toxicity. Their dysregulation may also confer pathogenic conditions in neurovascular diseases. A better understanding of their expression patterns and functions has uncovered the potential use of these riboregulators as neuroprotectants to antagonize the detrimental molecular events taking place upon ischemic-reperfusion injury. In this review, we discuss the various roles of non-coding RNAs in brain development and their mechanisms of gene regulation in relation to ischemic brain injury. We will also address the future directions and open questions for identifying promising non-coding RNAs that could eventually serve as potential neuroprotectants against ischemic brain injury.

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Late preconditioning with isoflurane in cultured rat cortical neurones

Cited by 33 publications

References 23 publications

Identification of miRNAs Involved in the Protective Effect of Sevoflurane Preconditioning Against Hypoxic Injury in PC12 Cells

Identification of miRNAs Involved in the Protective Effect of Sevoflurane Preconditioning Against Hypoxic Injury in PC12 Cells

The Effect of Specialist Neurosciences Care on Outcome in Adult Severe Head Injury

Non-Coding RNAs as Potential Neuroprotectants against Ischemic Brain Injury

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