Sevoflurane Preconditioning Downregulates GRIA1 Expression to Attenuate Cerebral Ischemia–Reperfusion-Induced Neuronal Injury

Li, Ye; Liang, Zhi; Lei, Shuyan; Wu, Xianren; Yuan, Tao; Ma, Kai; Chi, Kui

doi:10.1007/s12640-022-00620-5

Cited by 5 publications

(4 citation statements)

References 30 publications

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“…Studies in vertebrates emphasize the neuroprotective advantages of GRIA1 downregulation. Furthermore, shifts in the GRIA1 to GRIA2 ratio are postulated to modulate the calcium permeability of CP-AMPAR ( Li et al, 2023 ). In our dataset, Cg GRIA2 shows a contrasting expression pattern under copper and lead exposure.…”

Section: Discussionmentioning

confidence: 99%

Unveiling the functional diversity of ionotropic glutamate receptors in the Pacific oyster (Crassostrea gigas) by systematic studies

Zhang,

et al. 2023

Front. Physiol.

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Ionotropic glutamate receptors (iGluRs), pivotal in mediating excitatory neurosignals within the central nervous system, are instrumental in environmental stress responses. In this investigation, 12 iGluRs identified in the Pacific oyster are herein designated as CgiGluRs, and further categorized into three distinct subfamilies based on their transmembrane domains. Cross-species evolutionary analysis unveiled a high degree of conservation in the sequence and structural attributes of these CgiGluRs. These receptors are ubiquitously distributed across various tissues, with pronounced expression in the oyster’s mantle, labial palps, and gills, underlining their integral role in the oyster’s environmental sensing mechanisms. Post the D-shaped larval stage, a marked upward trend in CgiGluRs expression was observed, denoting their critical involvement in oyster development beyond this phase. Exposure to five metals—cadmium (Cd), copper (Cu), zinc (Zn), mercury (Hg), and lead (Pb)—elicited a significant upregulation of CgGRIA4 expression, indicating a robust response to metal stress. A KEGG enrichment analysis on 142 genes, exhibiting parallel expression trends with CgGRIA4 under metal stress, suggests that CgGRIA4 could augment excitatory signal transmission by activating glutamatergic and dopaminergic synapses, thereby contributing to the metal stress response in the oyster. This inquiry not only bolsters our comprehension of the iGluRs gene family in metal stress response but also paves the way for future exploration of its cardinal role in cellular signaling and environmental adaptability.

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Section: Discussionmentioning

confidence: 99%

Unveiling the functional diversity of ionotropic glutamate receptors in the Pacific oyster (Crassostrea gigas) by systematic studies

Zhang,

et al. 2023

Front. Physiol.

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“…Sevoflurane might exert beneficial effects on cerebral IR-induced neuronal injury through inhibiting the surface expression of the glutamate receptor 1 and blocking CP-AMPAR (calcium permeble-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor). Halothane is hepatotoxic; therefore, its clinical utility is limited, despite the eventual neuroprotective effect [ 43 , 44 ].…”

Section: Cross Tolerancementioning

confidence: 99%

Ischemic Tolerance—A Way to Reduce the Extent of Ischemia–Reperfusion Damage

Burda

Bürda

Morochovič

2023

Cells

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Individual tissues have significantly different resistance to ischemia–reperfusion damage. There is still no adequate treatment for the consequences of ischemia–reperfusion damage. By utilizing ischemic tolerance, it is possible to achieve a significant reduction in the extent of the cell damage due to ischemia–reperfusion injury. Since ischemia–reperfusion damage usually occurs unexpectedly, the use of preconditioning is extremely limited. In contrast, postconditioning has wider possibilities for use in practice. In both cases, the activation of ischemic tolerance can also be achieved by the application of sublethal stress on a remote organ. Despite very encouraging and successful results in animal experiments, the clinical results have been disappointing so far. To avoid the factors that prevent the activation of ischemic tolerance, the solution has been to use blood plasma containing tolerance effectors. This plasma is taken from healthy donors in which, after exposure to two sublethal stresses within 48 h, effectors of ischemic tolerance occur in the plasma. Application of this activated plasma to recipient animals after the end of lethal ischemia prevents cell death and significantly reduces the consequences of ischemia–reperfusion damage. Until there is a clear chemical identification of the end products of ischemic tolerance, the simplest way of enhancing ischemic tolerance will be the preparation of activated plasma from young healthy donors with the possibility of its immediate use in recipients during the initial treatment.

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“…Sevoflurane (Sevo), a frequently used volatile anesthetic, has been verified to alleviate I/R injury in multiple vital organs, including the lungs, 4 the brain, 5 and the heart 6 . In our previous report, we found that Sevo preconditioning downregulated the expression of glutamate receptor 1 to reduce cerebral I/R‐induced neuronal injury 7 . In this research, we aimed to decipher the mechanism underlying Sevo in alleviating hepatic I/R injury.…”

Section: Introductionmentioning

confidence: 99%

“…6 In our previous report, we found that Sevo preconditioning downregulated the expression of glutamate receptor 1 to reduce cerebral I/R-induced neuronal injury. 7 In this research, we aimed to decipher the mechanism underlying Sevo in alleviating hepatic I/R injury.…”

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confidence: 99%

Sevoflurane blocks KLF5‐mediated transcriptional activation of ITGB2 to inhibit macrophage infiltration in hepatic ischemia/reperfusion injury

Li,

Gao,

Lei

et al. 2024

The Journal of Gene Medicine

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BackgroundSevoflurane (Sevo) preconditioning and postconditioning play a protective role against injury induced by hepatic ischemia/reperfusion (I/R). At the same time, the involvement of macrophage infiltration in this process and the precise mechanisms are unclear. Here, we designed this research to elucidate the protective effects of Sevo against hepatic I/R injury and the molecules involved.MethodsThe alleviating effect of Sevo on the liver injury was analyzed by liver function analysis, hematoxylin and eosin staining, Masson trichrome staining, terminal deoxynucleotidyl transferase‐mediated 2′‐deoxyuridine 5′‐triphosphate nick end labeling, western blot analysis and an enzyme‐linked immunosorbent assay. An in vitro cell model was developed using alpha mouse liver 12 (AML12) cells, and the cell model was treated with oxygen–glucose deprivation and reoxygenation and Sevo. Multiple bioinformatics databases were used to screen transcriptional regulators related to hepatic I/R injury and the targets of Krueppel‐like factor 5 (KLF5). KLF5 expression was artificially upregulated alone or with integrin beta‐2 (ITGB2) knockdown to substantiate their involvement in Sevo‐mediated hepatoprotection.ResultsSevo protected the liver against I/R injury by reducing cell apoptosis and inflammatory response. KLF5 was upregulated in liver tissues following I/R injury, whereas KLF5 overexpression aggravated macrophage infiltration and liver injury induced by I/R injury. KLF5 bound to the promoter of ITGB2 to enhance ITGB2 transcription. Knockdown of ITGB2 reversed the aggravation of injury caused by KLF5 overexpression in mice and AML12 cells.ConclusionsSevo blocked KLF5‐mediated transcriptional activation of ITGB2, thereby inhibiting macrophage infiltration in hepatic I/R injury.

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Sevoflurane Preconditioning Downregulates GRIA1 Expression to Attenuate Cerebral Ischemia–Reperfusion-Induced Neuronal Injury

Cited by 5 publications

References 30 publications

Unveiling the functional diversity of ionotropic glutamate receptors in the Pacific oyster (Crassostrea gigas) by systematic studies

Unveiling the functional diversity of ionotropic glutamate receptors in the Pacific oyster (Crassostrea gigas) by systematic studies

Ischemic Tolerance—A Way to Reduce the Extent of Ischemia–Reperfusion Damage

Sevoflurane blocks KLF5‐mediated transcriptional activation of ITGB2 to inhibit macrophage infiltration in hepatic ischemia/reperfusion injury

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