Hypothermic preconditioning but not ketamine reduces oxygen and glucose deprivation induced neuronal injury correlated with downregulation of COX-2 expression in mouse hippocampal slices

Jiang, Shan; Wu, Yong; Fang, De-fang; Chen, Ying

doi:10.1016/j.jphs.2018.04.001

Cited by 6 publications

(3 citation statements)

References 39 publications

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“…Contradictory to the findings that detected slower changes of brain diffusivity in AQP4 −/− during acute ischemia in vivo (Yao et al, 2015;Hirt et al, 2017;Chmelova et al, 2019), we did not observe a similar influence of AQP4 deletion during OGD in situ (Chmelova et al, 2019). This could be associated with the previously seen protective effect of hypothermic (32-33 • C) preconditioning that is present in situ (Jiang et al, 2018;Kreisman et al, 2020). Moreover, we previously demonstrated that severe pathological conditions are needed to reveal the role of AQP4 in cell swelling (Dmytrenko et al, 2013;Anderova et al, 2014).…”

Section: The Simultaneous Deletion Of Aqp4 and Trpv4 Block Changes Of...contrasting

confidence: 69%

The absence of AQP4/TRPV4 complex substantially reduces acute cytotoxic edema following ischemic injury

Suchá

Heřmanová

Chmelova

et al. 2022

Front. Cell. Neurosci.

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IntroductionAstrocytic Aquaporin 4 (AQP4) and Transient receptor potential vanilloid 4 (TRPV4) channels form a functional complex that likely influences cell volume regulation, the development of brain edema, and the severity of the ischemic injury. However, it remains to be fully elucidated whether blocking these channels can serve as a therapeutic approach to alleviate the consequences of having a stroke.Methods and resultsIn this study, we used in vivo magnetic resonance imaging (MRI) to quantify the extent of brain lesions one day (D1) and seven days (D7) after permanent middle cerebral artery occlusion (pMCAO) in AQP4 or TRPV4 knockouts and mice with simultaneous deletion of both channels. Our results showed that deletion of AQP4 or TRPV4 channels alone leads to a significant worsening of ischemic brain injury at both time points, whereas their simultaneous deletion results in a smaller brain lesion at D1 but equal tissue damage at D7 when compared with controls. Immunohistochemical analysis 7 days after pMCAO confirmed the MRI data, as the brain lesion was significantly greater in AQP4 or TRPV4 knockouts than in controls and double knockouts. For a closer inspection of the TRPV4 and AQP4 channel complex in the development of brain edema, we applied a real-time iontophoretic method in situ to determine ECS diffusion parameters, namely volume fraction (α) and tortuosity (λ). Changes in these parameters reflect alterations in cell volume, and tissue structure during exposure of acute brain slices to models of ischemic conditions in situ, such as oxygen-glucose deprivation (OGD), hypoosmotic stress, or hyperkalemia. The decrease in α was comparable in double knockouts and controls when exposed to hypoosmotic stress or hyperkalemia. However, during OGD, there was no decrease in α in the double knockouts as observed in the controls, which suggests less swelling of the cellular components of the brain.ConclusionAlthough simultaneous deletion of AQP4 and TRPV4 did not improve the overall outcome of ischemic brain injury, our data indicate that the interplay between AQP4 and TRPV4 channels plays a critical role during neuronal and non-neuronal swelling in the acute phase of ischemic injury.

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Section: The Simultaneous Deletion Of Aqp4 and Trpv4 Block Changes Of...contrasting

confidence: 69%

The absence of AQP4/TRPV4 complex substantially reduces acute cytotoxic edema following ischemic injury

Suchá

Heřmanová

Chmelova

et al. 2022

Front. Cell. Neurosci.

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“…In addition, an increased amount of Ni 2 O 3 has been reported to contribute to an increased work function (WF) . The peaks at 531.7 and 532.1 eV are related to NiOOH. − The higher binding energy at 533 eV is attributed to hydroxyl (OH) groups, and the intensity of this peak increases after the treatment, which is probably because of the hydroxyl group present in the MeO-2PACz structure.…”

Section: Resultsmentioning

confidence: 99%

Surface Passivation of Sputtered NiO_x Using a SAM Interface Layer to Enhance the Performance of Perovskite Solar Cells

et al. 2022

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Sputtered NiO x (sp-NiO x ) is a preferred hole transporting material for perovskite solar cells because of its hole mobility, ease of manufacturability, good stability, and suitable Fermi level for hole extraction. However, uncontrolled defects in sp-NiO x can limit the efficiency of solar cells fabricated with this hole transporting layer. An interfacial layer has been proposed to modify the sp-NiO x /perovskite interface, which can contribute to improving the crystallinity of the perovskite film. Herein, a 2-(3,6-dimethoxy-9 H -carbazol-9-yl)ethyl]phosphonic acid (MeO-2PACz) self-assembled monolayer was used to modify an sp-NiO x surface. We found that the MeO-2PACz interlayer improves the quality of the perovskite film due to an enlarged domain size, reduced charge recombination at the sp-NiO x /perovskite interface, and passivation of the defects in sp-NiO x surfaces. In addition, the band tail states are also reduced, as indicated by photothermal deflection spectroscopy, which thus indicates a reduction in defect levels. The overall outcome is an improvement in the device efficiency from 11.9% to 17.2% due to the modified sp-NiO x /perovskite interface, with an active area of 1 cm 2 (certified efficiency of 16.25%). On the basis of these results, the interfacial engineering of the electronic properties of sp-NiO x /MeO-2PACz/perovskite is discussed in relation to the improved device performance.

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“…A brief cycle of HP applied before an ischemia-reperfusion episode significantly decreased both damage and oxidant indicators while increasing antioxidant levels in isolated perfused rat liver [30]. Jiang et al (2018) showed that the downregulation of COX-2 expression and the increase of Na + /K + ATPase activity increase tolerance to hypoxic damage and may be associated with the effectiveness of mild HP at 33 °C [31]. These results show that HP might be a promising strategy in protecting the brain against hypoxic damage.…”

Section: Discussionmentioning

confidence: 99%

Iron homeostasis is altered in response to hypoxia and hypothermic preconditioning in brain glial cells

Aral¹,

Ergün²,

Engin³

et al. 2020

Turk J Med Sci

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Background/aim: Altered iron metabolism is one of the pathophysiological mechanisms occurring during hypoxic injuries in the central nervous system. Proper homeostasis of cellular iron is regulated by iron import, storage, and export proteins that prevent excess iron overload or iron starvation in cells. Therapeutic hypothermia is an approved treatment for hypoxic ischemia in newborns, but the underlying molecular mechanism is still unknown. We studied the effects of hypoxia, preceded with preconditioning, on the iron homeostasis of glial cells, known as a major actor in the inflammatory process during perinatal brain injury.Materials and methods: Primary microglia and astrocytes in culture were exposed to 12 h of hypoxia with or without mild hypothermic preconditioning. The mRNA expression was assessed using qPCR. Iron accumulation was visualized via modified Perl's histochemistry. Cytokine levels in cell cultures were measured using ELISA.Results: Hypothermic preconditioning enhanced microglial viability, which previously was decreased in both cell types due to hypoxia. Hypoxia increased iron accumulation in the mixed glial cells and in ferritin expression in both microglia and astrocytes. Hypotermic preconditioning decreased the elevated ferritin-light chain expression significantly in microglia. Iron importer proteins, DMT1 and TfR1, both increased their mRNA expression after hypoxia, and hypothermic preconditioning continued to support the elevation of DMT1 in both glial cell types. Ferroportin expression increased as a survival factor of the glial cell following hypoxia. Hypothermic preconditioning supported this increase in both cell types and was especially significant in astrocytes. IL-10 levels were prominently increased in cell culture after hypothermic preconditioning. Conclusion:The data suggest that hypothermic preconditioning affects cellular iron homeostasis by regulating the storage and transfer proteins of iron. Regulation of the cellular iron traffic may prevent glial cells from experiencing the detrimental effects of hypoxia-related inflammation.

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Hypothermic preconditioning but not ketamine reduces oxygen and glucose deprivation induced neuronal injury correlated with downregulation of COX-2 expression in mouse hippocampal slices

Cited by 6 publications

References 39 publications

The absence of AQP4/TRPV4 complex substantially reduces acute cytotoxic edema following ischemic injury

The absence of AQP4/TRPV4 complex substantially reduces acute cytotoxic edema following ischemic injury

Surface Passivation of Sputtered NiO_x Using a SAM Interface Layer to Enhance the Performance of Perovskite Solar Cells

Iron homeostasis is altered in response to hypoxia and hypothermic preconditioning in brain glial cells

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Hypothermic preconditioning but not ketamine reduces oxygen and glucose deprivation induced neuronal injury correlated with downregulation of COX-2 expression in mouse hippocampal slices

Cited by 6 publications

References 39 publications

The absence of AQP4/TRPV4 complex substantially reduces acute cytotoxic edema following ischemic injury

The absence of AQP4/TRPV4 complex substantially reduces acute cytotoxic edema following ischemic injury

Surface Passivation of Sputtered NiOx Using a SAM Interface Layer to Enhance the Performance of Perovskite Solar Cells

Iron homeostasis is altered in response to hypoxia and hypothermic preconditioning in brain glial cells

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Surface Passivation of Sputtered NiO_x Using a SAM Interface Layer to Enhance the Performance of Perovskite Solar Cells