Wnt/β-catenin signaling pathway contributes to isoflurane postconditioning against cerebral ischemia-reperfusion injury and is possibly related to the transforming growth factorβ1/Smad3 signaling pathway

Zhang, Guixing; Ge, Ming; Han, Zhaobin; Wang, Sheng; Yin, Jiangwen; Li, Peng; Xu, Feng; Zhang, Qingtong; Dai, Zhijun; Xie, Liping; Li, Yan; Si, Jun‐Qiang; Ma, Ketao

doi:10.1016/j.biopha.2018.11.143

Cited by 28 publications

(25 citation statements)

References 33 publications

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“…A permanent model of middle cerebral artery occlusion (MCAO) was established according to the previously reported Longa method [20,21], using 32 male Sprague-Dawley (SD) rats (aged 6-8 weeks, initial weight 200 ± 15 g, Shanghai Sippr Bk Laboratory Animals Co., Ltd., Shanghai, China) as previously reported [22]. The rats used in the experiment were housed under specificpathogen-free (SPF) conditions in a 12-h light/dark cycle, with free access to food and water.…”

Section: Rat Middle Cerebral Artery Occlusion Model Establishment Andmentioning

confidence: 99%

“…An incision measuring 1.5 cm was cut along the midline of the head to expose the skull around the Bregma. According to the stereotactic atlas of the rat, a trocar was inserted into the lateral ventricle (0.8 mm posterior to the Bregma, 1.5 mm next to the midline, 4.0 mm below the outer surface of the skull) [21]. The trocar was reserved for further use.…”

Section: Rat Middle Cerebral Artery Occlusion Model Establishment Andmentioning

confidence: 99%

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RETRACTED ARTICLE:Bone mesenchymal stem cell-derived exosomal microRNA-29b-3p prevents hypoxic-ischemic injury in rat brain by activating the PTEN-mediated Akt signaling pathway

Hou¹,

Li²,

Zhao³

et al. 2020

J Neuroinflammation

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Background: Mesenchymal stem cells (MSCs) are suspected to exert neuroprotective effects in brain injury, in part through the secretion of extracellular vesicles like exosomes containing bioactive compounds. We now investigate the mechanism by which bone marrow MSCs (BMSCs)-derived exosomes harboring the small non-coding RNA miR-29b-3p protect against hypoxic-ischemic brain injury in rats. Methods:We established a rat model of middle cerebral artery occlusion (MCAO) and primary cortical neuron or brain microvascular endothelial cell (BMEC) models of oxygen and glucose deprivation (OGD). Exosomes were isolated from the culture medium of BMSCs. We treated the MCAO rats with BMSC-derived exosomes in vivo, and likewise the OGD-treated neurons and BMECs in vitro. We then measured apoptosis-and angiogenesis-related features using TUNEL and CD31 immunohistochemical staining and in vitro Matrigel angiogenesis assays. Results: The dual luciferase reporter gene assay showed that miR-29b-3p targeted the protein phosphatase and tensin homolog (PTEN). miR-29b-3p was downregulated and PTEN was upregulated in the brain of MCAO rats and in OGD-treated cultured neurons. MCAO rats and OGD-treated neurons showed promoted apoptosis and decreased angiogenesis, but overexpression of miR-29b-3p or silencing of PTEN could reverse these alterations. Furthermore, miR-29b-3p could negatively regulate PTEN and activate the Akt signaling pathway. BMSCs-derived exosomes also exerted protective effects against apoptosis of OGD neurons and cell apoptosis in the brain samples from MCAO rats, where we also observed promotion of angiogenesis.Conclusion: BMSC-derived exosomal miR-29b-3p ameliorates ischemic brain injury by promoting angiogenesis and suppressing neuronal apoptosis, a finding which may be of great significance in the treatment of hypoxic-ischemic brain injury.

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Section: Rat Middle Cerebral Artery Occlusion Model Establishment Andmentioning

confidence: 99%

Section: Rat Middle Cerebral Artery Occlusion Model Establishment Andmentioning

confidence: 99%

RETRACTED ARTICLE:Bone mesenchymal stem cell-derived exosomal microRNA-29b-3p prevents hypoxic-ischemic injury in rat brain by activating the PTEN-mediated Akt signaling pathway

Hou¹,

Li²,

Zhao³

et al. 2020

J Neuroinflammation

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“…The Wnt/b-catenin signaling pathway was downregulating by hypoxia-ischemia in H9C2 cells (Tao et al, 2016) and its dysfunction in temporal lobe epilepsy is responsible of structural and functional abnormalities, while restoring Wnt pathway leads to neuroprotective effects (Huang et al, 2015). Similarly, the neuroprotective effects of isoflurane PostC is mediated by Wnt/b-catenin signaling in MCAO models of cerebral ischemia in rats (Zhang et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Tolerance Induced by (S)-3,5-Dihydroxyphenylglycine Postconditioning is Mediated by the PI3K/Akt/GSK3β Signalling Pathway in an In Vitro Model of Cerebral Ischemia

Gerace

Scartabelli

Pellegrini‐Giampietro

et al. 2020

Neuroscience

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Ischemic postconditioning (PostC) is an endogenous neuroprotective strategy for cerebral ischemia induced by low activation of glutamate receptors. We have previously shown that the application of the mGluR1/5 agonist (S)-3,5-dihydroxyphenylglycine (DHPG) 5 min after 30 min of oxygen and glucose deprivation (OGD) reduces CA1 damage in organotypic hippocampal slices by activating the PI3K-Akt signalling pathway. In order to extend these data, we analysed the production of reactive oxygen species (ROS) and the glycogen synthase kinase 3b (GSK3b) signalling pathway. Our results show that DHPG PostC was associated with a reduction in the formation of ROS that is massively increased 24 h after OGD exposure. This reduction was prevented by the PI3K inhibitor LY294002, indicating that there is a link between the PI3K/Akt pathway and the formation of ROS in the protective mechanisms of PostC. DHPG PostC also induces a transient increased in GSK3b phosphorylation and inactivation that is followed by nuclear accumulation of b-catenin, that probably lead to the upregulation of neuroprotective genes. Our results propose GSK3b as new target for neuroprotection, therefore, we verified that the two GSK3b inhibitors N-(3-Chloro-4-methylphenyl)-5-(4-nitrophenyl)-1,3,4-oxadiazol-2-amine (TC-G 24) and LiCl are neuroprotective agents in OGD and also can be used as PostC agents.

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“…A possible explanation of this effect is that β-catenin regulates the expression of B-cell lymphoma 2 (Bcl2), a protein with anti-apoptotic properties [147]. Interestingly, post-conditioning with isoflurane reduced the infarction volume and apoptosis of neurons in rats, and this effect was linked to Wnt signaling activation [148]. Since elevated plasma levels of Dkk1 were observed in humans after stroke [149], we hypothesize that similar mechanisms might occur in the human brain.…”

Section: The Impact Of Wnt Signaling On Different Cell Types During Imentioning

confidence: 89%

Glia and Neural Stem and Progenitor Cells of the Healthy and Ischemic Brain: The Workplace for the Wnt Signaling Pathway

Knotek

Janečková

Kriška

et al. 2020

Genes

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Wnt signaling plays an important role in the self-renewal, fate-commitment and survival of the neural stem/progenitor cells (NS/PCs) of the adult central nervous system (CNS). Ischemic stroke impairs the proper functioning of the CNS and, therefore, active Wnt signaling may prevent, ameliorate, or even reverse the negative effects of ischemic brain injury. In this review, we provide the current knowledge of Wnt signaling in the adult CNS, its status in diverse cell types, and the Wnt pathway’s impact on the properties of NS/PCs and glial cells in the context of ischemic injury. Finally, we summarize promising strategies that might be considered for stroke therapy, and we outline possible future directions of the field.

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Wnt/β-catenin signaling pathway contributes to isoflurane postconditioning against cerebral ischemia-reperfusion injury and is possibly related to the transforming growth factorβ1/Smad3 signaling pathway

Cited by 28 publications

References 33 publications

RETRACTED ARTICLE:Bone mesenchymal stem cell-derived exosomal microRNA-29b-3p prevents hypoxic-ischemic injury in rat brain by activating the PTEN-mediated Akt signaling pathway

RETRACTED ARTICLE:Bone mesenchymal stem cell-derived exosomal microRNA-29b-3p prevents hypoxic-ischemic injury in rat brain by activating the PTEN-mediated Akt signaling pathway

Tolerance Induced by (S)-3,5-Dihydroxyphenylglycine Postconditioning is Mediated by the PI3K/Akt/GSK3β Signalling Pathway in an In Vitro Model of Cerebral Ischemia

Glia and Neural Stem and Progenitor Cells of the Healthy and Ischemic Brain: The Workplace for the Wnt Signaling Pathway

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